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Transcript
MASARYK UNIVERSITY
Faculty of Medicine
STOMATOLOGY
FOR STUDENTS OF GENERAL MEDICINE
Supplement to the university textbook
Professor MUDr. Jiří Vaněk, CSc. et al.
BRNO 2009
STOMATOLOGY
FOR STUDENTS OF GENERAL MEDICINE
Authors:
Professor MUDr. J. Vaněk, CSc.
Professor MUDr. A. Fassmann, CSc.
Professor MUDr. L.Izakovičová-Hollá, CSc.
Professor MUDr. A Vašků, CSc.
Doc. MUDr. M. Machálka, CSc.
Doc. MUDr. L. Roubalíková, Ph.D.
MUDr. L. Procházková, CSc.
MUDr. P. Prachár, Ph.D.
MUDr. S. Bartáková, Ph.D.
MUDr. O. Bulik, Ph.D.
MUDr. P.Černochová, Ph.D.
MUDr. H. Poskerová
MUDr. P. Augustín
MUDr. J. Šoukalová
MUDr. R. Gaillyová
© Professor MUDr. Jiří Vaněk, CSc. et al.
Brno 2009
ISBN..............................
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MASARYK UNIVERSITY, FACULTY OF MEDICINE
STOMATOLOGY
FOR STUDENTS OF GENERAL MEDICINE
CONTENTS ____________________________________________________________________
1. Stomatology, dental medicine, oral health (J. Vaněk) ...............................................................
1.1 Dental medicine .....................................................................................................................
1.2 Orthodontics ..........................................................................................................................
1.3 Maxillofacial surgery ............................................................................................................
2. Fundamentals of conservative dentistry (L. Roubalíková) .......................................................
2.1 Dental caries (caries dentis) ..................................................................................................
2.1.1 Introduction ...............................................................................................................
2.1.2 Etiology and pathogenesis of dental caries ...............................................................
2.1.3 The development and clinical signs of dental caries .................................................
2.1.4 Diagnosis and treatment of dental caries ...................................................................
2.2 Dental pulp diseases ..............................................................................................................
2.2.1 Characteristics and pathological conditions of dental pulp .......................................
2.2.2 Pulpitis, causes, symptoms ........................................................................................
2.2.3 Treatment of pulpitis .................................................................................................
2.3 Diseases of the periodontium ................................................................................................
2.3.1 Charakteristika a klasifikace periodontitid ................................................................
2.3.2 Treatment of periodontitis .........................................................................................
2.4 Focal infections of odontogenic origin ..................................................................................
2.5 Non-carious changes in dental tissue ....................................................................................
2.5.1 Congenital changes ...................................................................................................
2.5.2 Acquired changes ......................................................................................................
2.5.2.1 Trauma .......................................................................................................
2.5.2.2 Abrasion, erosion, wedge-shaped defects ..................................................
3. Diseases of the periodontium (P. Augustín) ................................................................................
3.1 Etiopathogenesis of prodontal diseases .................................................................................
3.1.1 Primary factor ............................................................................................................
3.1.2 Secondary factors ......................................................................................................
3.2 Classification of marginal periodontopathies ........................................................................
3.2.1 Classification of gingival diseases ............................................................................
3.2.2 Classification of periodontitis (localized and generalized) .......................................
3.2.3 Classification of atrophic changes in the periodontium ............................................
3.3 Mucogingival recessions .......................................................................................................
4. Diseases of the oral mucosa (H. Poskerová) ................................................................................
4.1 Anatomy and histology of the oral mucosa ...........................................................................
4.1.1 Masticatory mucosa...................................................................................................
4.1.2 Lining mucosa ...........................................................................................................
4.2 The properties of the oral mucosa .........................................................................................
4.3 Examination of the oral cavity .............................................................................................
4.4 Basic mucous efflorescence ..................................................................................................
4.5 Supplementary diagnostic tests .............................................................................................
4.6 Etiology of diseases of the oral mucosa ................................................................................
4.6.1 Physical and chemical factors ...................................................................................
4.6.2 Infectious factors .......................................................................................................
4.6.3 Allergic effects ..........................................................................................................
4.6.4 Autoimmune diseases ................................................................................................
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4.6.5 Stomatitis involving immune reactions .....................................................................
4.6.6 Disorders of mineral and vitamin metabolism ..........................................................
4.6.7 Endocrinopathy .........................................................................................................
4.6.8 Internal diseases ........................................................................................................
4.6.9 Blood diseases ...........................................................................................................
4.7 Selected diseases of the oral mucosa .....................................................................................
5. Guided tissue regeneration in periodontics (A. Fassmann).......................................................
5.1 Guided tissue regeneration ....................................................................................................
5.2 Thrombocyte-rich plasma in the treatment of bone defects ..................................................
5.3 Growth factors contained in platelet alpha-granules .............................................................
5.4 Conclusion .............................................................................................................................
6. Prosthetic dentistry (S. Bartáková) .............................................................................................
6.1 Biological factor ....................................................................................................................
6.2 Classification of abutment teeth ............................................................................................
6.3 Classification of dental defects..............................................................................................
6.4 Class I replacements according to Voldřich .........................................................................
6.4.1 Metal cap ...................................................................................................................
6.4.2 Ceramic cap ...............................................................................................................
6.4.3 Resin cap ...................................................................................................................
6.4.4 Facet crown ...............................................................................................................
6.4.5 Dowel crown .............................................................................................................
6.4.6 Bridges ......................................................................................................................
6.5 Class II replacements according to Voldřich ........................................................................
6.5.1 The replacement body ...............................................................................................
6.5.2 Fixation elements ......................................................................................................
6.5.3 Connecting elements .................................................................................................
6.5.4 Stabilization elements ...............................................................................................
6.6 Class III replacements according to Voldřich .......................................................................
7. Orthodontics (P. Černochová) .....................................................................................................
7.1 Internal factors – inheritance .................................................................................................
7.2 External factors .....................................................................................................................
7.2.1 External factors acting during the intrauterine development ....................................
7.2.2 External factors acting during the postnatal development ........................................
7.3 Prevention and prophylaxis of orthodontic abnormalities ....................................................
8. Diseases of jaw bones (M. Machálka) ..........................................................................................
8.1 Osteopathy .............................................................................................................................
8.1.1 Polyostotic osteopathy...............................................................................................
8.1.2 Monoostotic osteodysplasia of jaws ..........................................................................
8.2 Disorders of the maturation of bone mass components ........................................................
8.3 Disorders of bone tissue caused by hormonal dysfunction ...................................................
8.4 Diseases of bone tissue caused by metabolic disorders ........................................................
8.5 Disorders of bone tissue formation caused by unknown factors ...........................................
8.6 Necroses and inflammations of jaws .....................................................................................
8.6.1 Bacterial ....................................................................................................................
8.6.2 After irradiation .........................................................................................................
8.6.3 Prevention of osteoradionecrosis ..............................................................................
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8.6.4 Chemical (drug-induced)...........................................................................................
8.7 Bone cysts..............................................................................................................................
8.8 Bone tumours ........................................................................................................................
9. Preprosthetic surgery of edentulous čelistí (L. Procházková) ...................................................
9.1 Preprosthetic corrections of alveolar processes of jaws ........................................................
9.1.1 Partial preprosthetic corrections of alveolar processes without apparent bone
tissue atrophy.............................................................................................................
9.1.2 Elevation of atrophic alveolar processes ..................................................................
9.1.2.1 Relative elevation of the the alveolar process ............................................
9.1.2.2 Absolute elevation of the alveolar process .................................................
9.1.3 Implantation procedures ............................................................................................
9.1.3.1 The augmentation of atrophic jaws of biocompatible materials derived
from hydroxyl apatite, tricalcium phosphate and bioglass .........................
9.1.1.2 Implantation procedures – enosseal dental implants ..................................
9.1.4 Segmental distraction osteogenessis .........................................................................
10. Jaw abnormalities (O. Bulik) .....................................................................................................
10.1 Etiology and classification of jaw abnormalities ..................................................................
10.2 Patient examination ...............................................................................................................
10.2.1 Examination of the patient’s general state of health .................................................
10.2.2 Examination of orofacial system ...............................................................................
10.3 Treatment of jaw abnormalities .............................................................................................
10.3.1 Le fort I line maxillectomy........................................................................................
10.3.2 Sagittal osteotomy of mandibular branches ..............................................................
10.4 Individual types of jaw abnormalities ...................................................................................
10.4.1 Class II jaw abnormalities .........................................................................................
10.4.2 Class III jaw abnormalities ........................................................................................
10.4.3 Jaw abnormalities in the vertical and horizontal planes ............................................
10.4.4 Post-cleft and post-traumatic deformities .................................................................
11. Biological and biophysical aspects of oral implantology (P. Prachár) ...................................
11.1 Biological properties .............................................................................................................
11.1.1 Biotolerant materials .................................................................................................
11.1.2 Bioinert materials .....................................................................................................
11.1.3 Bioactive materials ....................................................................................................
11.2 Mechanical physical properties .............................................................................................
11.2.1 Material with excellent m-p properties ....................................................................
11.2.2 Materials with satisfactory m-p properties ...............................................................
11.2.3 Materials with poor m-p properties ..........................................................................
11.3 The use of dental implants in other indications .....................................................................
11.4 Augmentation – replacement, tissue restoration ...................................................................
11.4.1 Augmentation methods ............................................................................................
11.4.2 Augmentation material .............................................................................................
12. Genetic aspects of diseases in the cranifacial region (L. Izakovičová-Hollá, J. Šoukalová,
R. Gaillyová, A. Vašků) .....................................................................................................................
12.1 Orthodontic abnormalities .....................................................................................................
12.1.1 Disorders of the dentition ..........................................................................................
12.1.2 Jaw abnormalities ......................................................................................................
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12.1.3 Cleft lip and palate ...................................................................................................
12.1.4 Some syndromes associated with cleft lip or cleft lip and palate..............................
12.1.4.1 Autosomal dominant inheritance ...............................................................
12.1.4.2 Autosomal recessive inheritance ................................................................
12.1.4.3 X-linked inheritance ...................................................................................
12.1.4.4 Congenital chromosomal aberrations .........................................................
12.1.4.5 Syndromes without non-Mendelian inheritance ........................................
12.2 Craniosynostoses and craniofacial syndromes ......................................................................
12.2.1 Craniosynostoses ......................................................................................................
12.2.2 Autosomal dominant inheritance ..............................................................................
12.2.3 Autosomal recessive inheritance ...............................................................................
12.2.4 Craniofacial syndromes .............................................................................................
12.3 Dental caries ..........................................................................................................................
12.4 Diseases of the periodontium ................................................................................................
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STOMATOLOGY
FOR STUDENTS OF GENERAL MEDICINE
1. STOMATOLOGY, DENTAL MEDICINE, ORAL HEALTH ________________________
Stomatology as medical field has more than a 100-year-long history in the Czech Republic. In the
1920s, it became part of university courses. Nowadays, it is a separate medical field that is studied
in a specific, accredited Master’s degree study programme, as provided by law, focussing on the
prevention, diagnosis, treatment and research into diseases and developmental disorders of teeth,
dentition and tissues in the oral cavity including adjacent organs and tissues. The term “dental
medicine” is being increasingly used instead of the term “stomatology”.
The main aim of current stomatology – dental medicine – is to ensure the adequate level of oral
health in all age categories of population. It is based on current scientific knowledge and on
internationally recognized programmes for improving the quality of health outlined in the
documents and objectives of the World Health Organization (WHO) for 2010, The Charter of
Rights and Freedoms, The Charter of Children’s Rights, etc. In this respect, it creates the
conditions for a systematic improvement in the quality of dental care and oral health for all
individuals.
The basic goal of dental medicine is to treat dental diseases using the most recent therapeutic
approaches, scientific knowledge and the results of research. Preventive care is a method that is
gaining more and more importance. It must be applied consistently and emphasize the role of
health consciousness of an individual and family, in accordance with the goals outlined in the
National Health Programme.
According to the basic concept of the Ministry of Health of the Czech Republic from 2001 and Act
No. 95/2004 Sb., stomatology - dental medicine – as a separate medical field consists of three
integral parts: dental medicine, orthodontics, maxillofacial surgery.
1.1 Dental medicine
With its therapeutic scope, dental medicine consists of five basic fields: conservative dentistry that
deals with the direct treatment of dental tissue; paediatric dental medicine that focuses on the
population of children and adolescents; periodontics and diseases of the oral mucosa that focuses
on the diseases and treatment of the dental tissue and oral mucosa; prosthetic dentistry that uses
different types of replacement to treat defects in the dentition, oral surgery and implantology that
focuses on the surgery of hard and soft tissues in the oral cavity at an outpatient level. These
branches of the field of dental medicine constitute the main topic of the curriculum of the Dental
Medicine pregraduate study programme which has been included in the programme of medical
faculties as a separate field since 2004. Dental medicine is studied five years in the Czech Republic
and is completely compatible with Dental Medicine study programmes within the EU. Dental
Medicine at the Faculty of Medicine, Masaryk University, has a total of 7 subjects (4 of which
specialize in dental medicine) and 4 subjects are general medical fields. A great emphasis is laid
upon practical tuition, particularly in dental fields. The pre-graduate course provides basic
knowledge in different fields such as orthodontics and maxillofacial surgery. After completing the
Master's degree study programme in Dental Medicine, students will obtain the title of MDDr.
(Medicinae Dentium Doctor) and can start to perform preventive, diagnostic, prosthetic activities
and treat abnormalities and diseases of teeth, mouth, jaws and adjacent tissue, in accordance with
Act No. 95/2004 Sb.
1.2 Orthodontics
Orthodontics – jaw orthopaedics – is a separate specialized field. It has a preventive character for
the function of the whole orofacial system. It deals with congenital and developmental defects of
the dentition and jaws, their abnormalities and varieties causing damage to oral health or affecting
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the mental state of an individual. The treated dentition and a good level of oral hygiene are main
prerequisites for orthodontic diagnostics and therapy. Diagnostic approaches are based on the
compulsory medical records made according to the established standards in orthodontics. Therapy
uses fixed and removable orthodontic appliances sometimes combined with surgical methods. The
main aim of orthodontic care is to achieve a correct relationship between jaws with the perfect
articulation of the dentition, regular dental arches, symmetric function of the orofacial system and
satisfactory facial aesthetics. Orthodontics is included as a distinct subject in the pre-graduate
course of the dental medicine study programme. In order to obtain professional competence for
performing independent activities in orthodontics, it is necessary to complete a three-year
specialized course with a special examination, and take part in continuing lifelong education in the
specialization.
1.3 Maxillofacial surgery
Maxillofacial surgery is also a specialization field. It deals with the treatment of surgical diseases
in the region of the head and neck, focussing on the narrow anatomical region of the oral cavity,
oropharyngus and upper neck, and organs functionally associated with this region (salivary glands).
Surgical treatment is a primary method used, being combined with concomitant procedures
(cytostatic therapy, rehabilitation, aesthetic correction). This also includes inpatient care, which is
an integral part of treatment. Maxillofacial surgery as a distinct subject-matter is also included in
Dental Medicine pre-graduate courses. Specialization in this field requires qualifications in the
field of general medicine. Specialized preparatory courses completed with an examination take five
years; in the case of the graduates of dental medicine they can take up to seven years.
Prevention using all available means to achieve and maintain optimum oral health is an important
part of care in all fields of stomatology – dental medicine is – as pointed out in the Introduction.
The comprehensive concept of prevention is based on the application of all available methods of
primary prevention (modern principles of oral hygiene, fluoride prevention, food and eating habits),
secondary prevention (regular examinations of the oral cavity and early proper dental treatment)
and tertiary prevention (complete treatment to prevent further damage to the oral cavity).
The main tasks of prevention as to maintaining the optimum level of oral health particularly focus
on dental caries and periodontopathies which have a character of a disease with massive incidence.
The monitoring of the rate of dental caries and periodontopathies is the most important (but not the
only) parameter indicating the state of oral health and is subjected to thorough and deep evaluation.
2. FUNDAMENTALS OF CONSERVATIVE DENTISTRY ____________________________
Conservative dentistry addresses the problem of dental caries, congenital and acquired defects of
hard dental tissues of non-carious origin, and the diseases of the dental pulp and periodontium.
2.1 Dental caries (caries dentis)
2.1.1 Introduction
Dental caries is the most common disease in the human population. It follows from anthropological
findings that dental caries occurred in man of the Old Stone Age, and its rate has increased with the
development of civilization throughout the history. Out of civilizational factors, changes in the
composition of a diet and the preparation of food (the increased consumption of sugars and soft
food) played a major role. Dental caries that is not diagnosed in time and treated properly leads to
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the inflammation of the dental pulp, resulting in the transmission of inflammatory changes into the
adjacent part of the periodontium, which may cause serious, life-threatening complications.
2.1.2 Etiology and pathogenesis of dental caries
Dental caries is a disease of microbial origin. It starts with the decalcification of hard dental tissues
by the action of acids produced from sugars contained in the food by micro-organisms present in
the oral cavity, followed by the decomposition of organic substances in the presence of proteolytic
microbes. The amount and quality of saliva is closely associated with the development of dental
caries. Saliva is secreted from large and small salivary glands. Most saliva (69%) of a total amount
of saliva is produced in the submandibular salivary gland (glandula submandibularis), less saliva
(26%) is secreted from the parotid gland (glandula parotis), whereas the sublingual salivary gland
(glandula sublingualis) together with small salivary glands produce the remaining 5%. The daily
production of saliva ranges between 800 and 900 ml per day, saliva secretion is affected by a
number of external and internal factors, particularly by a diet.
More than 99% of saliva is water, the remaining 0.7% is solid substances of which 0.5% are
organic substances and 0.2% are inorganic substances. Inorganic substances present in saliva are
calcium, magnesium, potassium and sodium cations, and phosphate, chloride, carbonate, rhodanide,
fluoride and iodide anions. Saliva also contains different organic substances such as mucoids,
mucopolysaccharides, albumins and globulins, urea, uric acid, creatinine and ammonia. It also
contains enzymes of which α – amylase (ptyalin) is the most important enzyme initiating the
digestion of polysaccharides, and the components non-specific immunity (lysozyme,
lactoperoxidase) and various admixtures of liquid components of a diet. Saliva also contains
corpuscular material consisting of residues of food, micro-organisms, small quantities of red and
white blood cells from the gingival sulcus and tonsils.
Saliva has both mechanical and chemical effects on dental tissues. The mechanical effect relies in
the diluting of the accumulated residues of food, the washing of the tooth surface and the formation
of biofilm (dental plaque). The larger amount of saliva has a more significant cleaning effect. The
viscosity of saliva is also important because thick mucinous saliva has a smaller cleaning effect.
The chemical effect of saliva is based on its buffer capacity. The carbonate buffer system in saliva
is very important as it maintains the pH of saliva in a range of 6.65–7.15, in spite of frequent
deviations associated with the intake of some foods and beverages. However, the pH on the surface
of teeth in the dental biofilm plays a key role in the formation of dental caries. Various ions such as
fluorides, calcium ions, phosphates can diffuse into the enamel from saliva, affecting its quality. As
mentioned above, micro-organisms (particularly those that accumulate on the surface of teeth
forming a dental biofilm, i.e. microbial dental coating, dental plaque) play a major role in the
formation and development of dental caries. This community of micro-organisms colonize the
dental surfaces with insufficient self-cleaning (i.e. habitual unclean places such as sockets and
grooves, the cervical zones of teeth and interdental space). The acquired pellicle, i.e. a thin layer of
precipitated glycoproteins from saliva, is formed which retains first micro-organisms that multiply.
This results in the formation of plaque micro-colonies to which other micro-organisms adhere (coaggregation). Within a few hours, the layer of plaque becomes continuous, accumulating new
microbial species such as rod-shaped and filamentous micro-organisms, increasing the portion of
anaerobes, in the course of time. The effective cleaning of teeth is the only reliable possibility of
removing the dental biofilm. Solid food has a wiping effect which is not sufficient.
Dental plaque contains a wide range of microbial species. Streptococcus sp., Lactobacillus sp. and
some Actionomycetes sp. are directly associated with the formation and development of dental
decay. Cariogenic Streptococcus sp. (particularly Streptococcus mutants) are dangerous because
they are able to adhere to smooth dental surfaces, ferment sugars to give rise to aggressive acids
and produce intracellular and extracellular polysaccharides. Intracelullar polysaccharides serve as a
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metabolic pool so that the fermentation of sugars giving rise to acids can also continue in the
absence of sugars in food. Extracellular polysaccharides contribute a great deal to adhesion on the
surface of teeth and the co-aggregation of other microbes. Some Streptococcus sp., Diplococcus sp.
and rod-shaped micro-organisms are able to produce intracellular polysaccharides.
The formation of dental caries depends on the presence of low-molecular-weight saccharides in a
diet. Mono-, di- and trisaccharides diffuse easily into the biofilm where they serve as a nutrient for
the above-mentioned micro-organisms. Their metabolic products include organic acids that cause
the pH to decrease inside the biofilm which initiates the decalcification of hard dental tissue.
Sucrose, lactose, fructose and glucose are the most harmful sugars. High-molecular-weight
saccharides such as starch or glycogen do not enter the biofilm and are non-cariogenic.
The formation of dental caries is a slow process. The intense metabolic activity taking place in the
biofilm results in continuous variations in the pH on the dental surface. A decrease in the pH to
critical values (4.5–5.5) will result in demineralization whereas an increase in the pH helps the
accumulation of minerals in the enamel and on its surface. Frequent attacks by acids and a longlasting decrease in the pH will result in the formation of dental caries.
2.1.3 The development and clinical signs of dental caries
Decalcification starts on the enamel surface, the original structure of enamel changes, the crystals
of hydroxyapatite loose the regular arrangement and the loss of minerals causes the enamel to
become “spongy”. In the beginning, when no defect is visible, the lesion is without cavity. With a
gradual loss of minerals, the enamel decomposes which results in a defect – dental cavity, i.e.
lesion with a cavity. The course of dental decay in dentin is faster than in the enamel since dentin
contains a lower amount of minerals. If the dental caries is not detected in its early stages, it will
enlarge. The carious lesion consists of caverns filled with micro-organisms that produce acids and
proteolytic enzymes. Dental caries can be divided according to different factors. Primary caries is
formed on the surface of a tooth that has not been treated; secondary caries is associated with the
filling that has been carried out. Workers in bakeries and mills exhibit dental caries due to
occupational exposure to sugar and flour dust that accumulate on the surface of their teeth. Such
dental caries usually occur around the dental necks. Carious cavities can be divided according to
their size or depth as follows: superficial caries (it only involves the enamel), medium caries (it
affects dentin) and caries in the vicinity of the dental pulp (it is in the close vicinity of the dental
pulp). Clinical symptoms depend on the size and localization of dental caries. Initial stages of
dental caries are completely asymptomatic. When cavitation occurs, the caries can manifest itself
by increased sensitivity to thermal (particularly cold) and chemical stimuli (sweet, salty and acidtasting foods and beverages), the adhesion of food or by sensitivity during biting when some food
is pressed into the carious cavity. If the caries is close to the dental pulp, the symptoms may be
severe but it is not always the case. The dental pulp can fight effectively against the spread of
dental caries by producing protective dentin at the place of the carious cavity. It is less permeable
and represents a barrier against penetrating harmful substances. Dental caries that were not treated
early will cause the inflammation of dental pulp (pulpitis).
2.1.4 Diagnosis and treatment of dental caries
The dental caries is usually diagnosed by visual and gentle tactile examination using a dental probe
at good lighting. Auxiliary methods include the examination of dental tissues with light, infrared
laser fluorescence and X-ray examination. The last two methods mentioned can help very
significantly to reveal dental caries in its early stage. Decision on the method of treatment is based
on a particular local finding and also on the level of oral hygiene and the patient’s general state of
health and his/her ability to cooperate. The early stages of caries (lesions without cavity) can be
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treated using non-invasive approaches that rely on thorough oral hygiene, local fluoridation, or
local application of minerals such as calcium and phosphates, the elimination of micro-organisms
using ozone or chlorhexidine. If a cavity occurs, dental caries must be treated by preparation
(“drilling”) and filling (“a filling”). The extent of preparation depends on the size of dental caries,
the level of oral hygiene and a filling material used. The preparation procedure must remove all
irreversibly damaged dental tissues, ensure the retention of a filling and the resistance of the treated
tooth. The cavity prepared is then filled with a filling material. Filling materials can be temporary
or permanent. Temporary fillings are used for the temporary closure of a cavity, for different
reasons. (For example, it is necessary to ensure that inflamed tissue will heal first, or the reaction
of the dental pulp has to be tested, etc.) Some temporary materials are used for multiple purposes.
Zinc oxide phosphate cement is one of the most frequently used materials. Besides the temporary
closure of a cavity, it is also used to make a support under the permanent filling or cement
prosthetic works. Until recently, it has also been used to fill the root canal prior to surgery (root tip
amputation). Zinc oxide sulfate cement (Fletcher) originally used as a frequent temporary material
has been replaced with materials intended for direct use that are based on gypsum and organic
cements (Cavit, Provimat). Permanent filling materials serve for the final closure of a cavity.
Fillings can be plastic or rigid (inlays). A plastic filling is applied into the cavity in a plastic state
and solidifies in the cavity. A rigid filling is made in a laboratory on the basis of an imprint and is
then fixed in the cavity using the suitable cement. Decision on a type of filling to be used is at the
dentist’s discretion. The basic requirement is that the filling must reconstruct the missing dental
tissue both anatomically and functionally. Plastic filling materials such as amalgam, composite
filling materials and glass-ionomer cements can be considered. Amalgam as an alloy of metals with
mercury is the oldest plastic filling material used in dental medicine. Specially purified mercury is
mixed with a dust of a metal alloy containing silver, tin and copper. Amalgam is used in locations
where it does not interfere aesthetically. If used in compliance with occupational safety rules, it is
safe and fillings are durable. Composite filling materials are a chemically bound combination of
cross-linked polymer with inorganic filler. They are mechanically resistant and stable in the
environment of the oral cavity. They adhere to dental tissues on the principle of mechanical
adhesion after the previous adhesive treatment of the enamel and dentin using adhesive systems.
Adhesive preparation includes the itching of the enamel and dentin using an acid (usually
orthophosphoric acid) to create a system of microscopic roughness which is subsequently filled
with other components of the binding system that copolymerize with the composite applied into the
cavity. Connection is seamless provided that standard dental practices have been observed.
Composite materials were originally developed as aesthetic materials for the frontal section of the
dentition. Currently, they can also be used in the lateral sections of the dentition. Some cements
used for the fixation of prosthetic replacements are also derived from composite materials. Glassionomer cements (glass-ionomer, glass-polyalkenoate cements) bond chemically to dental tissues,
their thermal expansion coefficient is close to that of dentin and they also release fluoride ions,
which prevents the development of secondary dental caries. However, they are not as mechanically
resistant as amalgams or composites and should only be applied in certain kinds of cavities. Some
glass-ionomer cements are also used in the filling of root canals, the covering of the surface of
teeth due to reduced sensitivity or in the cementing of prosthetic works.
Rigid fillings – inlays – are made of noble metal alloys, ceramics or a composite. Their preparation
is demanding.
2. 2 Dental pulp diseases
2.2.1 Characteristics and pathological conditions of the dental pulp
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The dental pulp (pulpa dentis) fills the pulp cavity and root canals of teeth. It consists of thin
ligament with numerous cells, vessels and nerves. The presence of a large amount of free nerve
endings causes extreme pain in the case of damage or injury. Odontoblasts are the most important
cells in the dental pulp, being located on the border between the dental pulp and dentin. They
produce dentin for their entire life. Their thin fibres span into dentin tubules (Tomes fibres). The
dental pulp also contains a large number of multipotent cells and stem cells which may
differentiate into other cell elements. Root canals communicate with the periodontium by means of
the apical foramen through which the nerve and blood vessels pass entering the dental pulp. There
are also additional canals that communicate with the periodontium, i.e. ramification. Inflammation
and trauma are the most common disease of the dental pulp. Degenerative diseases of the dental
pulp are only of limited clinical significance.
2.2.2 Pulpitis, causes, symptoms
From a pathological - histological point of view, the inflammations of the dental pulp (pulpitis) can
be divided into subgroups, which is of very limited importance for clinical practice. One important
thing is to distinguish on the basis of a clinical finding whether or not a particular disease is
reversible. The inflammation of the dental pulp is usually caused by the spread of infection from
dental caries or a traumatic defect in the dental crown. Microbes can also penetrate into the pulp
via the apical foramen or ramifications in the case of periodontal pockets or rarely due to bacteria
present in blood (bacteremia). The dental pulp can also be damaged chemically by filling materials
applied into the close vicinity of the dental pulp, or thermally (in the case of vast and unsupported
amalgam filings or metal inlays).
The inflammation of the dental pulp is accompanied with typical spontaneous pain that occurs in
the form of attacks, usually at night or any time during the day. Initially, the episodes of pain are
short and can easily be relieved by analgesics. Later, the intensity of pain increases, and intervals
between attacks become shorter. Pain is neuralgiform and spreads into the surrounding regions of
the head and neck. The patient is usually unable to identify the tooth that causes the pain. This is a
source of diagnostic problems. The GP often refers the patient to a neurologist without
consideration that pain may be associated with teeth. After elapsing a differently long period of
time, the inflammation has spread in the apical direction from the dental pulp to the periodontium.
The sensitivity of the tooth upon chewing or percussion is detected (pulpal-periodontal syndrome).
The tooth affected with the inflammation of the dental pulp shows significant sensitivity to thermal
and chemical stimuli. Pain persists for several minutes or attacks of neuralgiform pain occur. If
pain is short-lasting and can be alleviated with analgesics, the disease is reversible. In the case of
long-lasting pain that cannot be alleviated with analgesics, being accompanied with percussion
sensitivity and a significant positive reaction to heat, the disease is irreversible.
2.2.3 Treatment of pulpitis
The treatment of pulpitis depends on a number of factors such as the importance of the affected
tooth in the dentition, patient compliance, the tooth’s condition (a degree of damage to the dental
crown, the anatomy of root canals, the condition of the periodontium), whether the disease is
reversible or irreversible. In the case of reversible disease, the indirect coverage of the dental pulp
is performed such that a small amount of a calcium hydroxide preparation is applied on the bottom
of the prepared cavity (but not directly on the pulp). This is covered by a support and filling.
Calcium hydroxide is in the form of a special cement or suspension. It alkalifies the pH of the
dental pulp that changed due to the inflammation and stimulates the formation of protective dentin.
If the pulpitis is irreversible, the dental pulp is removed after the administration of a local
anaesthetic (extirpation) and the root canal is filled with a root filling (usually gutta-percha
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combined with a specific root filling based on epoxy resins, glass-ionomer cement, etc.). Only in
exceptional cases, the dental pulp is necrotized by inserting a specific necrotizing agent before
extirpation (sporadic cases in which the administration of a local anaesthetic is contraindicated).
The exstirpation of the dental pulp and the root canal filling is then performed at the next visit to a
dentist.
2.3 Diseases of the periodontium
2.3.1 Characteristics and classification of periodontitis
The spread of inflammation from the dental pulp into the periodontium causes a disease called
periodontitis (apical periodontitis). Periodontitis can be caused by trauma or the chemical irritation
of the periodontium with substances inserted in the root canal. Inflammatory changes are initially
limited only to the close surroundings of the apex (the periodontal stage). Later, inflammation will
gradually spread into adjacent tissues (the enosseal phase), penetrating under the periosteum (the
subperiosteal phase) and mucosa after the necrosis of the periosteum (the submucosal phase).
Periodontitis may be acute or chronic. Chronic periodontitis can start and become acute any time
(chronic acutely exacerbated periodontitis). Unlike chronic periodontitis that is usually clinically
silent manifesting itself by occasional pain upon chewing or percussion, acute and acutely
exacerbated chronic periodontitis is characterized by severe pain. Patients identify the painful tooth
that is always sensitive to chewing and percussion, and often report a feeling of a protruding tooth
and shooting pain. Examination usually reveals the presence of swollen soft tissue or a fistula with
the leak of purulent exudate, in the vicinity of the tooth. Regional lymph nodes can also be swollen
and the organism may show general alteration. Periodontitis in the subperiostal and submucous
phases is accompanied with facial swelling. Subperiostal and submucous abscess is characterized
by fluctuation upon palpation. The subperiosteal phase is the most painful whereas pain relief is
observed in the submucous phase. X-ray examination is a valuable tool to complete the
examination. Acute periodontitis is usually characterized by enlarged periodontal fissure whereas
chronic periodontitis shows brightening adjacent to the apical region which may have distinct
borders (periodontitis circumscripta) or vague contours (periodontitis diffusa). There is granulation
tissue in this region, often containing the patches of epithelium originating from the stage of
development, i.e. epithelial cell rests of Malassez. The proliferation of such epithelial cells may
give rise to a radicular cyst.
2.2.2 Treatment of periodontitis
An approach to therapy is based on the evaluation of the importance of the causal tooth to the
dentition, the anatomy of the tooth (the treatability of root canals, the condition of periodontium, an
extent of damage to the dental crown), the patient’s general state of health and compliance. The
trepanning of a pulp cavity – the opening of the pulp cavity and the cleaning of the root canal - will
bring immediate pain relief to a patient with acute periodontitis as it will release the exudate. After
acute symptoms disappear, endodontic treatment is performed. It includes the removal of infected
mass from the pulp cavity and root canals, the enlargement and hermetic filling of root canals. The
same procedure is applied in the case of chronic periodontitis where the acute phase is missing. If
root canals are accessed to entirely and filled, one can expect the consolidation of tissues in the
vicinity of the apex, the healing of fistula and bone apposition. Surgical intervention will not be
neecessary. The subperiosteal and submucous forms usually require an incision and the
prescription of antiobiotics in the case of the general alteration of the organism. Surgical solution
such as the amputation of the root apex or hemiextraction as a supplement to conservative therapy
depends on the outcome of endodontic treatment. In the absence of problems, surgery can be
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performed in at least 6 months. Conservative treatment can be performed either at a single visit or
at multiple visits with intervals allowing to filling the root canal with a paste containing calcium
hydroxide. The final filling of the root canal is made using gutta-percha combined with a plastic
root filling as mentioned in the previous chapter. Extraction is an alternative to the conservative
approach. It is performed after the careful consideration of all indications. Inflammation that has
spread beyond the periodontal fissure can have one serious complication which is the propagation
of inflammation into the space around the jaws and the development of inflammation around the
jaws which is life-threatening for a patient. Such cases require immediate cooperation with a
dentists specialized in dental surgery. The causal tooth will always be extracted, the patient will be
given antibiotics and the incision of abscesses and wound drainage will be necessary.
2.4 Focal infections of odontogenic origin
This includes a group of diseases in distant organs which are caused by the presence of a focus of
infection in the oral cavity. It is assumed that micro-organisms, toxins and other substances
produced during tissue decomposition are spread via blood and cause a secondary disease in distant
parts and organs of the body. In fact, every chronic inflammation can be a focus of infection. Focal
infection that is particularly dangerous is subacute bacterial endocarditis because it can develop
after the extraction of a root with a focus of infection. This also applies to other diseases such as
eye diseases, nervous diseases and joint diseases. Among the most common sources of infection in
the oral cavity are devitalized teeth, the inflammation of dental pulp, periodontal pockets or
abscesses, odontogenic cysts, retained dental roots, the inflammations of jaw cavities and serious
gingival inflammations. It is not simple to make a diagnosis. It is necessary to identify the main
cause of problems and analyse the ontogenetic finding. The patient history has to include clinical
examinations, including X-ray exam, even in the case of toothless jaws. Treatment is based on the
elimination of an infectious agent. The method of treatment is decided on the basis of the extent of
suspicion of focal infection and the seriousness of the finding. If focal infection is suspected, the
easiest way of eliminating chronic inflammation is by extracting the tooth. At the same time, the
patient is treated for a disease of an essential organ. Extraction is performed under the antibiotic
screen. Patients who have recently undergone heart surgery or angiosurgical intervention and
patients with congenital and acquired defects of the immune system are very prone to bacteremia.
Less serious diseases may not require extraction; high-quality endodontic treatment or therapy of
gingivitis is recommended in such cases.
2.5 Non-carious changes in dental tissue
2.5.1 Congenital changes
Inheritance or the presence of harmful substances is affecting the development of dental tissue play
an important role in congenital defects. Amelogenesis imperfecta is one of the best known
congenital defects - the enamel has various defects such as staining or it can be so soft that it will
abrade soon after tooth eruption and disappear. Dentinogenesis imperfecta is characterized by the
brownish colour of teeth and the early obliteration of the pulp cavity. Hereditary damage to the
enamel and dentin can be part of general diseases such as osteogenesis imperfecta (teeth have
brownish or pink-brown colour, the pulp cavity is missing, roots are short), etc.
Different harmful substances acting during tooth development can cause defects in the formation of
hard dental tissue. Inflammation around the germ of a permanent tooth, general diseases
accompanied with fever, the excessive intake of fluorides and tetracycline antibiotics are the most
common causes of defects in dental tissue mineralization and production. The enamel shows
whitish, yellowish or brownish spots, holes, grooves or zones. Teeth damaged by tetracycline
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antibiotics are characterized by noticeable yellow discolouration. Therapy is based on aesthetic
correction using composite materials or on prosthetic treatment.
2.5.2. Acquired changes
2.5.2.1 Trauma
Trauma may involve the dental crown, root canal, periodontium or a combination of all these
structures. The method of treatment depends on the size of a defect and a degree of risk to the
dental pulp. This may include single reconstruction, the treatment of the dental pulp using calcium
hydroxide and the application of a filling, or the extirpation of the dental pulp is performed
followed by the filling of the root canal. Fractures of the root and injuries to the periodontium
require the splinting of teeth and also endodontic treatment using the shaping effect of calcium
hydroxide applied as a temporary root filling which is repeatedly restored, before the root canal is
finally filled.
2.5.2.2 Abrasion, erosion, wedge-shaped defects
Abrasion is the extreme wear of teeth due to traumatic bite or bad habits. Erosion is a loss of dental
tissue caused by acids contained in beverages with the low pH (for example Coca –Cola, juices
etc.) or due to decalcification caused by stomach acid in patients with mental anorexia or
gastroesophageal reflux disease. People working with acids in chemical plants often show defects
due to dental erosion. These defects are usually detected in the cervical region. Wedge-shaped
defects are also localized in the cervical region of teeth, being characterized by smooth surface.
Factors contributing to their formation include abrasion and the uneven load of teeth that causes the
small particles of the enamel to break off. Treatment of these defects relies on the elimination of
causes and the replacement of lost dental tissue with suitable filling materials.
3. DISEASES OF THE PERIODONTIUM __________________________________________
3.1 Etiopathogenesis of periodontal diseases
3.1.1 Primary factor
Microbial layer on the surface of teeth (plaque, biofilm) is soft, structurally organized,
accumulates on the surface of a tooth and cannot be removed by rinsing.
Bacteria in dental plaque have different properties that may accelerate the destruction of the
periodontium. Their enzymes such as collagenases, hyaluronidases and chondroitinsulfatases
dissolve intercellular mass and collagen structures and facilitate the penetration of bacteria into
tissue. Tissues are also damaged by the products of bacterial metabolism, for example ammonia,
indole and hydrogen sulphide. Bacteria produce specific toxins. Endotoxins are
lipopolysaccharides originating from the wall of Gram-negative bacteria and cause inflammatory
reaction. Exotoxins (for example leukotoxin) are antigens released by bacteria.
3.1.2 Secondary factors
Local factors – cause damage to tissues indirectly by affecting the accumulation of plaque or by
direct mechanical traumatization (for example supra and subgingival plaque, the abnormal
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configuration of teeth, etc.). Mechanical traumatization is also of iatrogenic origin (for example
orthodontic movement of teeth, the overhanging margins of crowns and fillings).
Systemic factors – congenital immunological diseases, syndromes (Down syndrome), diseases
caused by metabolic disorders (diabetes mellitus), autoimmune diseases.
3.2 Classification of marginal periodontopathies
Current classification with international validity was established in 1999.
3.2.1 Classification of gingival diseases
A. Dental plaque-induced gingival diseases – gingivitis induced only by dental plaque and
gingival diseases modified by general factors (for example gingivitis gravidarum, gingival
hypertrophy caused by some drugs).
B. Non-plaque-induced gingival diseases:
Gingival diseases caused by specific bacteria (N. gonorrhoe, T. pallidum), viruses (infections
caused by herpetic viruses), yeast (candidosis) and symptoms of general diseases of the gingiva
(lichen planus, pemphigoid).
3.2.2 Classification of periodontitis (localized and generalized)
A. Non-aggressive periodontitis
B. Aggressive periodontitis
C. Periodontitis as a manifestation of general diseases (blood diseases, genetic diseases (Down
syndrome, Papillon-Lefévre syndrome, histiocytosis X)
D. Necrotizing periodontal diseases (NPD)
E. Abscesses of periodontal tissue (gingival, periodontal, pericoronal abscess)
F. Periodontitis associated with endodontic lesions (endodontic-periodontal lesion)
3.2.3 Classification of atrophic changes in the periodontium
localized and generalized gingival recesses
3.3 Mucogingival recessions
belong to a group of non-inflammatory periodontopathies. The recession of the gingiva occurs
from the vestibular side of the jaw, in combination with other factors (rough oral hygiene,
unsuitable hygienic aids, injuries, orthodontic treatment, occlusal trauma, etc.).
Therapy – the correction of oral hygienic habits, proper choice of tooth cleaning techniques and the
correction of the articulation of the dentition or surgical correction.
4. DISEASES OF THE ORAL MUCOSA ___________________________________________
4.1 Anatomy and histology of the oral mucosa
From a topographical - anatomical point of view, the mucosa can be divided into buccal mucosa,
labial mucosa, alveolar mucosa, the mucosa of hard and soft palate (including the uvula and
palatine arches), the mucosa of the oral cavity base, tongue base and of the dorsum of the tongue.
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The oral mucosa is covered by stratified squamous epithelium, its properties differ by function, i.e.
by a load to which it is exposed.
4.1.1 Masticatory mucosa
(the mucosa of the hard palate, gingiva and the dorsum of the tongue).
It is covered with the stratified squamous keratinizing epithelium. The epithelium forms
duplicatures on the dorsum of the tongue - papillae which are the basis of the physiological coating
of the tongue and accommodate taste receptors.
4.1.2 Lining mucosa
(buccal mucosa, labial mucosa, alveolar mucosa, the mucosa of the soft palate, the base of the oral
cavity and the base of the tongue) is coated by the non-keratinized epithelium.
The red mucosa of the lip is a specific type of the keratinized mucosa on the border between the
skin and the oral cavity. It does not contain skin adnexa (sweat gland, hair follicles) or tiny salivary
glands which lead to its increased sensitivity and vulnerability.
Stratified squamous epithelial cells are attached to the basal membrane which separates the
epithelium from the lamina propria (lamina propria mucosae). This changes into the submucossal
tissue (except for the section of the dorsum of the tongue where it is firmly attached to aponeurosis
linguae), or into the periosteal tissue (hard palate, connected gingiva). The lamina propria (lamina
propria mucosae) consists of thin collagen tissue, elastic fibres, cellular elements (fibroblasts,
fibrocytes, histiocytes, heparinocytes) and contains blood and lymphatic vessels, nerve endings.
The submucosal tissue contains a large amount of tiny salivary glands.
4.2 The properties of the oral mucosa
– good mechanical resistance, very good healing properties, rich blood supply, dense neural
network with specific elements (mechanoreceptors, chemoreceptors), some absorption ability
4.3 Examination of the oral cavity
The colour of mucosa
physiological – light pink (race-dependent and individual deviations dependent on the amount of
melanin)
enhanced paleness – anaemia, white – hyperkeratosis, reddened – inflammations, yellowish –
hepatitis, pigmentation – external (tattooing using metals, intoxication with Pb, Hg, Ag), internal –
melanin, haemoglobin
The humidity of the mucosa
healthy mucosa is always wet
reduced humidity (hyposalivation) – severe fever, NPB, coma, intoxication with atropin,
xerostomia caused by some drugs, sicca syndrome, Sjögren syndrome.
increased humidity (drooling, ptyalism) – intoxication with Hg, Pb, As, inflammations, nervous
system disorders, mouth disease
The thickness of the mucosa
enlargement (hyperplasia) – irritation, hormonal effects, effects of drugs, tumour growth
reduction (atrophy) – vitamin B, Fe, oestrogen deficiency, Sjögren syndrome.
4.4 Basic mucous efflorescence
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Primary: macula – spot, papule – bud, tuber– bump, vesicle – blister, pustule – a blister filled with
pus
Secondary: cracked skin, fissure, squama - scale, crust, eschar, erosion – a superficial epithelial
defect, ulcer, tumour
4.5 Supplementary diagnostic tests
They serve to verify and clarify clinical diagnoses, and establish the sensitivity of an infectious
agent to some drugs such as antibiotics or antimycotics.
Haematological tests – to exclude the possibility of a general disease
Immunological tests – in the case of chronic and recurrent conditions
Microbiological tests (virological, bacteriological, mycological) – to determine the ethiological
agent of a disease. Direct examination (microscopic, cultivation), or indirect (serological)
Biopsy – to confirm a clinical diagnosis, due to differentially diagnostic reasons
a) Histopathological examination
b) Determination of autoimmune diseases using direct and indirect immunofluorescence
4.6 Etiology of diseases of the oral mucosa
The causes of diseases of the oral mucosa are very varied and can be local and general, or external
and internal.
4.6.1 Physical and chemical factors
a) Mechanical – such as the traumatization of the oral mucosa
b) Thermal – heat (burning) or cold
c) Radiation – UV radiation (actinic cheilitis), X-ray overdose, radiation due to accidents with
radiation sources
d) Galvanic – the presence of some metals can induce galvanic irritation (metal acts as an
electrode, saliva acts as electrolyte)
e) Chemical burns caused by exposure to acids or bases (accidents, treatment, suicide)
f) The effects of drugs – toxic, allergic, toxoallergic
4.6.2 Infectious factors
a) Viral infections (herpes gingivostomatitis, herpes stomatitis, herpes labialis, HIV, hand-foot and
mouth disease, herpangina, herpes zooster, infectious mononucleosis, varicella, measles)
b) Bacterial infections (gingivitis ulceroza, specific inflammations – syphilis, tuberculosis)
c) Fungal infections (oral candidiasis, other fungal infections)
4.6.3 Allergic effects
Drug-induced stomatitis (stomatitis medicamentosa) – anaphylactic reaction
Contact allergy (stomatitis venenata) – food allergens, cosmetic products, mouthwashes, pastes,
locally applied drugs, dental materials
4.6.4 Autoimmune diseases
Pemphigus vulgaris, mucous pemphigoid, lupus erythematosus, Sjögren syndrome
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4.6.5 Stomatitis involving immune reactions
Recurrent aphtae, oral lichen planus, erythema exsudativum multiforme Hebrae
4.6.6 Disorders of vitamin and mineral metabolism
Deficiency in vitamins A, B (B12 pernicious anaemia), C (scurvy)
Disorders in iron metabolism (sideropenic anemia, Plummer-Vinson syndrome)
4.6.7 Endocrinopathy
Diabetes mellitus, adrenal gland hypofunction (Addison’s disease), thyroid gland hypofunction or
hyperfunction
4.6.8 Internal diseases
Liver diseases, digestive system diseases (ulcerous colitis, Crohn’s disease), kidney diseases
(uremic stomatitis)
4.6.9 Blood diseases
Bleeding diseases (hemorrhagic diathesis)
– thrombocytopathy (thrombocytopenia, thrombasthenia), – vasculopathy, – coagulopathy
(congenital - haemophilia, acquired - anticoagulation therapy)
White blood cell disorders – leukaemia, agranulocytosis
Red blood cell disorders – anaemia (Fe and B12 deficiency)
4.7 Selected diseases of the oral mucosa
are described in the following university textbooks:
1) Stomatologie pro studující všeobecného lékařství (Stomatology for students of general
medicine), Team of authors, Brno 1996, Faculty of Medicine, Masaryk University Brno
2) Repetitorium onemocnění sliznice dutiny ústní (vybrané kapitoly), (Revision manual of diseases
of the oral mucosa (selected chapters)), Lydie Izakovičová Hollá, Antonín Fassmann, Brno 2003,
Faculty of Medicine, Masaryk University Brno
5. GUIDED TISSUE REGENERATION IN PERIODONTICS (GTR) ___________________
5.1 Guided tissue regeneration
Guided tissue regeneration is a progressive surgical method to create the new investing and
supporting structure of teeth (the periodontium) affected by periodontitis (reattachment). This
means the complete regeneration of periodontal tissue including dental root cement, the alveolar
bone, the periodontium and the epithelial attachment to the tooth.
This new principle of surgical therapy of periodontitis is based on the mechanical prevention of
access of epithelial ligament cells of the gingiva and oral epithelial cells to the periodontal defect.
Subsequently, this enables progenitor cells (desmodonts which are able to differentiate) to grow in
and colonize the defect. Periodontal fibres contain desmodonts, i.e. cells with a regenerating and
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differentiating potential which are the only cells capable of restoring the periodontium destroyed
by periodontitis.
This is achieved by the placement of an occlusal membrane to form the space between the
membrane and the surface of the root to which the tissue of the periodontium can grow in. The
membrane also prevents the proliferation of gingival connective tissue and epithelium to the
surface of the root during healing.
The resorbable Bio-Gide membrane is used in guided tissue regeneration in periodontics. It
consists of pure collagen and has two layers. One layer is porous and is applied to the bone to
allow its growth into the defect. The mucoperiosteal flap is applied over the other more compact
layer of the membrane to prevent soft tissue from growing in the treated wound. The membrane
maintains its structure in wet conditions and should be used in combination with supportive
materials (such as natural inorganic bone matrix of bovine origin) to fill the defect. In periodontics,
the Bio-Oss granulate is used alone or in a mixture with 10% of collagen fibres (Bio-Oss Collagen).
The outcome of the surgery (the restoration of periodontal structures of the supporting system
(reattachment) and bone tissue growth examined by radiography) is assessed after nine months.
On the basis of the biological principle of guided tissue regeneration, a new concept called guided
bone regeneration was developed. It is based on a hypothesis that different kinds of cells multiply
and compete during the early stages of wound healing. The barrier membrane is used to prevent
undesirable cells from growing in and proliferating. As a result, this will favour the cells that have
ability to regenerate the particular type of tissue.
5.2 Thrombocyte-rich plasma in the treatment of bone defects
The update of GTR and GBR is based on the introduction of a tissue engineering method to induce
tissue regeneration using thrombocyte-rich plasma. The easiest technique to achieve tissue
regeneration is to apply growth factors at the place where the differentiation and proliferation of
cells is required.
Growth factors can be obtained from autologous Platelet Rich Plasma (PRP) using separation
instruments.
By using this technology, the number of platelets in PRP can increase three times, which also
increases the local concentration of growth factors.
5.3 Growth factors contained in platelet alpha granules
•
•
•
•
•
Platelet-Derived Growth Factor (PDGF)
Transforming Growth Factor β 1 (TGF- β 1)
Transforming Growth Factor β 2 (TGF- β 2)
Vasculat Endothelial Growth Factor (VEGF)
Epithelial Growth Factor (EGF)
In dental surgeries associated with bone tissue replacement in periodontics, maxillofacial and
dentoalveolar surgery, the PRP is applied in a mixture with the Bio-Oss inorganic bone material in
the form of composite gel.
For these purposes and with regard to the extent of a defect, it is sufficient to use 3 ml of PRP
mixed with 1 gram of the Bi- o-Oss granulate, followed by the addition of 1 ml of thrombin and 1
ml of calcium chloride. This will provide a composite implantation gel that contains high levels of
growth factors and can easily be applied to a particular bone defect.
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5.4 Conclusion
Regeneration results in the formation of tissue that is structurally and functionally identical to
original tissue. The main aim of surgical procedures on the periodontium is to induce the
regeneration of the investing and supporting system of teeth, including the alveolar bone and root
cement, and the subsequent formation of the functional periodontal ligament within 6 months. This
also increases their therapeutic effect.
6. PROSTHETIC DENTISTRY ___________________________________________________
Prosthetic dentistry focuses on the replacement of the dental crown, the entire tooth or several teeth,
the parts of alveolar processes and soft tissues in the mouth or face. Dental replacements serve to
restore the original function of the dentition, phonation and aesthetics. Prosthetic replacements can
be fixed or removable. According to the distribution of chewing pressure, individual dental
replacements can be divided into three groups: replacements with the dental, dentomucous or
mucous distribution of pressure.
6.1 Biological factor
Teeth to which prostheses (dental replacements) are attached are called abutment teeth. They are
usually part of fixed bridges, with interlink between them, or can be located at the defect’s margins
to ensure the fixation of a dental replacement. Abutment teeth may differ in quality, which is
expressed by the biological factor of abutment teeth that specifies whether the tooth will be part of
the fixed (bridge) or removable replacement. There are several factors that can affect the biological
factor of a tooth: the size of the carious focus, the place of the carious focus, the fracture of the
dental crown involving the enamel, dentin or the pulp cavity of the tooth that will require
endodontic treatment of the dental root. Another factor affecting the quality of teeth is the
endodontic treatment of the tooth, the number of teeth that underwent endodontic treatment, and
the subsequent development of periapical lesions, i.e. granuloma on the roots. The quality of
alveolar bone resorption that can be horizontal, vertical, stepwise or dish-shaped is of key
importance. The presence of loose teeth is also included in the biological factor. Besides all abovementioned factors, any dental deformations are also monitored, for example root curvature, root
fracture, poor endodontic treatment of the tooth performed by a previous dentist, the calcification
of the pulp, odontoma, and dens invaginatus. All these factors contribute to the biological factor of
the tooth which is determined by visual examination or by using examination tools (dental probe,
mirror, and forceps) and particularly by radiography. An OPG image (orthopantomogram) is made
at the first patient’s visit, or alternatively, a large number of small intra-oral images are made.
Proper dental hygiene in a patient plays an important role. The biological factor together with the
plan of prosthetic treatment in a particular patient is finally established on the basis of the OPG
which rules out pathological processes in the jaw alveolus. According to the OPG and clinical
examination of the dentition, it is decided which teeth or roots will be extracted or undergo
endodontic treatment to be saved. In some cases, teeth will undergo preventive endodontic
treatment; the patient will use temporary replacement (fixed or removable) only for the duration of
dental treatment.
6.2 Classification of abutment teeth
Class I – First and second molars, canines, two Class II abutments as an equivalent, third molar
only in exceptional cases
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Class II – Premolars, upper big incisors, this group can also include the third molar, depending on
its biological factor
Class III – Small upper incisors, all lower incisors, third molar with the poor biological factor
Classes of abutments make sense for the determination of the extent of fixed replacement.
Abutment teeth of bridges must have a Class I abutment on both sides of the space, with interlink
between them. If a Class II abutment was used as a tooth, this would result in its overload. There
must be two Class II teeth on one side and one Class I abutment on the other. Two Class II teeth
are equivalent to one Class I tooth.
Missing teeth are defects of the dentition that can also be divided into groups. The best known
classification in the Czech Republic is the Voldřich classification or the Kennedy classification
adopted from the European Union.
6.3 Classification of dental defects
According to the number of defects, the Voldřich classification divides the dentition into the
following classes: Class I (dentition with gaps) – the dental distribution of chewing pressure,
defects are treated using fixed and removable bridges, Class II (shortened dental arch) the
dentomucous distribution of chewing pressure, defects are treated using skeletal replacements of
the dentition, Class III (major defects), i.e. residual dentition where the defect cannot be classified
in Class I or Class II, defects are treated using removable replacements with the mucodental
distribution of chewing pressure, or Class IV – complete dental replacement with the mucous
distribution of chewing pressure.
Fig. 1. Scheme of Class I according to Voldřich.
a) A defect with the loss of one or two teeth
b) A defect with the loss of 3 - 4 teeth defined as a large gap
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Fig. 2. Scheme of Class II according to Voldřich.
Types of the shortened dental arch:
a) Bilateral shortened dental arch
b) Unilateral shortened dental arch
c) Unilateral shortened dental arch with gaps,
d) Bilateral shortened dental arch with gaps in the frontal segment – adapted according to Voldřich
et al.
Fig. 3. Scheme of Class III according to Voldřich – residual dentition
Prosthetic work can be made directly in the patient’s mouth (direct procedure), for example the
shaping of root extension in the patient’s mouth, or indirectly (indirect procedure) where the
patient’s dental defect is imprinted in the dental surgery room. The laboratory technician will cast
the imprint in the laboratory and make a preliminary model using the models of teeth in both jaws
on the basis of the wax bite imprint. The dental replacement is made subsequently by using a
laboratory procedure.
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6.4 Class I replacements according to Voldřich
Fixed replacements
Abutment structures include inlays, onlays, root inlays, crowns and bridges. The inlay replaces part
of the lost crown (for illustration: a filling in the tooth crown which is made of gold (in the past) or
ceramics (today)). The onlay replaces the occlusal part of the crown including tubercles, either
partially or completely, and one or both of its proximate parts (it used to be made of gold in the
past; it is currently made of ceramics). The root inlay or root extension replaces the whole dental
crown and is fixed using a root peg inserted into the endodontically treated root canal and
cemented using dental cements. Root inlays are then covered with crowns. Crowns are used to
replace the whole clinical damaged dental crown.
Types of crowns:
6.4.1. Metal cap
This type of a crown is made of different metal alloys (usually gold, gold-palladium or silverpalladium). The preparation of the abutment tooth is shoulderless. The dentist will make the
imprints of the patient’s lower and upper jaw, one using the alginate-based imprint material, the
other using the silicone imprint materials (detailed imprint) and determine the relationship between
both jaw using the wax bite imprint. Imprints will then be sent to the laboratory where the
laboratory technician will cast the imprints and make plaster models of the upper and lower jaws
which will be used to fabricate the wax model of the crown on the basis of preliminary factory wax
moulds. The wax model is then cast from the alloy using the lost wax method. The cast metal
crown is shaped and polished. The dentist will then attach the crown using dental cements. One
major disadvantage of metal caps is that they are not aesthetic and are only intended for use in the
distal parts of the dentition.
6.4.2 Ceramic cap
– aesthetic crown. Preparation to the rectangular shoulder. The laboratory technician will make
plaster models on the basis of silicone imprints and the wax bite imprint. A platinum foil is applied
on the abutment followed by the gradual application of several layers of ceramics whose colour
corresponds to that of dentin or enamel. One particular colour shade is applied on the proximal
surface of the tooth; the other colour shade is applied on the enamel layer. A transparent shade is
applied on the incisal edge. Finally, a glaze is applied. After burning in a furnace, the platinum foil
is removed. The ceramic cap is attached to the reduced tooth stump using dental cement. The main
advantage of the ceramic cap is that it has a natural discolouration and glaze which does not
accumulate microbial plaque. However, demanding fabrication of the abutment tooth and the
fragility of the cap are major disadvantages of ceramic crowns.
Analogously, the ceramic crown can also be fabricated by applying the ceramic material on the
ceramic shell rather than on the platinum foil, as described above.
There are also other types of ceramic crowns, for example ceramic crowns shaped from ceramic
blocks, i.e. the CAD-CAM system. The optical imprint obtained using an infrared camera
connected to a computer or scanner is used to make a virtual working model that serves to make a
design of a crown which is then fabricated from a preliminary factory-made ceramic mould using
the computer-controlled instrument.
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6.4.3 Resin cap
– this type of crowns is used by dentists as a temporary or permanent crown. It consists of
methylmetacrylate or composite resin. The main disadvantage of these crowns is that they are
fragile and their colour is unstable. After some time, they may cause the inflammation of gums
(gingivitis).
6.4.4 Facet crown
– facet crowns can be metal, cast, or combined crowns, with the aesthetic facet usually made of
resin or composite resin. The preparation of the abutment is on the curved shoulder. The metal
structure is used to cover the surface of a tooth with an internal cap whereas the outer resin layer
completes the shape of the crown from the vestibular side. Facet crowns are usually made of gold
alloys. The simple preparation of a tooth is the main advantage. One major disadvantage is that
plastics are prone to discolouration by pigments contained in food, coffee, wine or nicotine.
6.4.5 Dowel crown
– this type of crowns is not practically used nowadays. It is based on root extension and the
application of a crown. The laboratory technician will make a resin facet on the vestibular side.
This crown is attached to the root dowel in the root canal using cement.
6.4.6 Bridges
Fixed replacements or bridges are supported by Class II abutment teeth with interlink between
them. Prior to the fabrication of the bridge, the abutment must be shaped into the exact
predetermined shape. Preparation will differ between individual teeth and will result in the
reduction of a tooth on which tubercles and fissures are prepared. Instruments for preparation are
made of diamond of different roughness or fineness. Preparation is started with large instruments;
the size of instruments gradually decreases. At the end, cutters are used to shape composites. The
basic types of the preparation of the abutment are: shoulderless preparation, preparation on the
rounded shoulder, and preparation on the rectangular shoulder. The gap that is replaced by interlink
is a gap of 1-4 teeth. If the bridge forms a line, it is called a linear bridge. When the lines
connecting individual teeth form a plane, the bridge is called the planar fixed bridge or splint
bridge. Interlink is firmly attached to the crowns on individual abutments. If the interlink is in
contact with the alveolar process, it is a contact interlink. If there is a gap between interlink and the
alveolar mucosa, interlink is called s rinsing interlink. Since the major emphasis is currently placed
on the aesthetics of replacements, contact interlinks are predominant. Compared to crowns, they
are reduced by one third on occlusion in order to lower the chewing pressure acting on the
abutment teeth.
Removable bridges are currently made only very rarely.
6.5 Class II replacements according to Voldřich
are based on removable replacements (with the dentomucous distribution of chewing pressure) that
are anchored using fixing elements on the outer teeth adjacent to the defect which have no fillings,
have been reduced by grinding the enamel, or have been crowned with clasp crowns. Partially
removable replacements of the dentition can be used to treat defects that cannot be treated using
fixed bridge.
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Basic elements of prostheses
6.5.1. The replacement body
– the saddle is made of methylmetacrylate, it replaces the missing part of the alveolus to which
resin and ceramic teeth are attached.
6.5.2. Fixation elements
– are structures that enable the prosthesis to be attached to the remaining dentition. Clasps or pushin connections are most common; telescopic or cone-shaped crowns are made very rarely. All
fixation elements described can be combined in order to treat different types of defects of the
dentition.
A. Clasps – types: wire, combined or cast. Wire clasps are made of a wire (0.7-0.8 mm in diameter),
cast clasps are made of chromium cobalt alloys. Their task is to attach the dental replacement to
crowns.
B. Telescope crowns – consist of two mantles, one mantle is cemented to the abutment tooth, the
other mantle is part of the removable replacement. There is usually a spring between both mantles
that fits into the groove on the internal mantle that is attached to the tooth by cement.
C. Conical crowns – are composed of two mantles, one mantle is cemented to the tooth, the other
mantle is part of the removable replacement. When the removable replacement is inserted, both
mantles are fixed by means of friction, no spring or push-in device are present.
D. Push-in attachment – push-in attachments are composed of two parts: the male component
(patrix) which is part of the tooth (crown or root inlay) is pushed out as a sphere or roller, and the
female component (matrix) which is part of the removable prosthetic replacement of the dentition
to fit the male component.
E. Connectors – connectors connect dental crowns between each other, being firmly attached to
them. They serve as a male component to which the female component (part of the removable
replacement) fits.
6.5.4. Connecting elements
– serve to connect individual parts of prostheses and are cast from chromium-cobalt alloy.
A. Frontal palatal connector – attaches the upper prosthesis in the region of palatal folds of the
hard palate
B. Lateral palatal connector – attaches the prosthesis in the upper jaw in the region of distal
segments of the dentition
C. Posterior palatal connector – attaches the removable prosthesis at the posterior margin of the
hard palate
D. Sublingual connector – fixes the left and right parts of the prosthesis body, is placed along the
lingual slope of the alveolar process of the lower jaw
E. Reduced palatal plate – is placed in the middle of the palate and replaces the frontal and
posterior palatal connector of the prosthesis.
6.5.5. Stabilization elements
– enhance the stability of the dental replacement and prevent the separation of the removable
replacement from the prosthetic bed.
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A. The stabilization arm of the clasp – is part of the clasp, runs along the maximum convexity of
the oral surface of the tooth.
B. Extended clasp – the extension of the stabilization shoulder of the clasp to the next tooth results
in the extended clasp.
C. Continuous clasp – connection between clasps at the left and right side of the alveolus results in
the continuous clasp.
6.6 Class III replacements according to Voldřich
This includes the residual dentition, for example there are one to three teeth located one next to
another or one against the other, and the respective defect does not belong to Voldřich Class I or II.
Depending on the biological factor, cast clasps are used in the case of a good biological factor, or
one-arm wire clasps in the case of an unsatisfactory biological factor which serves as a transition to
complete dental replacement. The distribution of chewing pressure is mucodental, i.e.
predominantly mucous. Replacements resemble total replacements. The plate denture with one or
more clasps is used. In some cases, the replacement can be attached using push-in connections
(male and female parts). The replacement body is made of methyl metacrylate to which teeth
usually made of resin are attached.
7. ORTHODONTICS ____________________________________________________________
Etiology of orthodontic abnormalities
Orthodontic abnormalities of various degrees of seriousness occur in 60 - 80 % of the population.
Orthodontic treatment is indicated in approximately 30 - 50 % of the population. There are many
different causes of orthodontic abnormalities and they usually combine. Generally, it is not
possible to determine the etiological factor of a particular orthodontic abnormality. Etiological
factors can be internal and external.
7.1 Internal factors – inheritance
The development of the dentofacial region is – to a great degree - determined genetically.
Polygenic inherited traits include the size and shape of teeth, the number of teeth, the position of
dental germs and the direction of their eruption, the period of tooth eruption, the size and shape of
jaws, the period and manner of the growth of jaws. These traits have their natural variability. In
addition, individual traits can be inherited independently one of the other.
The contribution of inheritance to the development of orthodontic abnormalities is very significant.
The same or similar abnormalities often occur in individual members of a particular family.
Typically inherited abnormalities include: right mandibular prognathism, closed bite, hypodontia
and hyperodontia, tooth retention, the abnormal configuration of individual teeth, distocclusion,
and clefts. Some types of clefts and other congenital syndromes (for example dysostosis
craniofacialis – Crouzon syndrome, dysostosis cleidocranialis) can also be caused by gene
mutations and chromosomal aberrations.
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7.2 External factors
7.2.1 External factors acting during the intrauterine development
The intrauterine development of the orofacial region can be affected by different substances with
teratogenic effects. Chemical teratogens particularly include pharmaceutical agents (cytostatics,
acetyl salicylic acid, diazepam, thalidomide etc.), alcohol (Foetal Alcohol Syndrome). Physical
teratogens include X-radiation. Infectious teratogens include cytomegalovirus, rubeola virus,
toxoplasmosis, influenza virus. If teratogens act in the first trimester, cleft lip and palate is the most
common sign of damage. Smoking is a major factor that has a teratogenic effect; the harmful effect
of chemicals contained in cigarette smoke and hypoxia may cause clefts in the orofacial region.
7.2.2 External factors acting during the postnatal development
Birth trauma – High obstetric forceps may result in the contusion of the jaw joint with subsequent
ankylosis and the destruction of the condylar cartilage. The growth of the lower jaw is seriously
affected, microgenia occurs, it results in the “bird face”.
Diet – In the past, breast-feeding was considered to have a beneficial effect on the growth of the
lower jaw because the infant will push the lower jaw forward when holding the nipple. However,
this effect was not statistically confirmed. Artificially fed children show a higher rate of bad habits.
Bad habits – Dummy or thumb sucking is the most common bad habit. Less frequent bad habits
include the sucking of the pillow’s corner, lower lip, or cheek, or the biting of nails, lips, tongue,
pencil or other objects. During thumb sucking, the thumb forces upper incisors into protrusion and
lower incisors into retrusion, the horizontally placed thumb results in open bite. The degree of the
abnormality depends on the duration of the bad habit during the day. Most children stop thumb or
dummy sucking before the age of 3 years. In some children, this bad habit persists to older age
(usually thumb sucking). Thumb sucking during sleep can also be found in adult patients with open
bite but it is very rare. It is very difficult to eliminate this involuntary action. If thumb sucking is
not eliminated, open bite is likely to recur after treatment.
The type of swallowing and the position of the tongue at rest – Two types of swallowing can be
recognized. Normal (adult) swallowing means that the teeth are pressed in the position of
maximum intercuspidation, with the tongue leaning against incisors and the frontal part of the
palate and then against the palate. Atypical (infant) swallowing means that the tongue is pressed
between incisors, leaning against the internal side of the lips, and the teeth are not in contact. This
type of swallowing was originally considered to be a causal factor of open bite. Nowadays, it is
assumed to be a consequence of open bite rather than its cause. The tongue can be a cause of open
bite if it is placed between the teeth while in the rest position, preventing the vertical development
and growth. This condition is observed in macroglossia.
Mouth breathing – Natural breathing in man is through nose. A healthy individual breathes
through the mouth only at increased physical exertion. Mouth breathing is observed in individuals
suffering with diseases of the upper airways (cold, allergic coryza, adenoid vegetation, other
obstructions of upper airways, for example deviated nasal septum). If mouth breathing persists in
older children, it will have a negative effect on the growth of the medium parts of the face and jaws.
During mouth breathing, the mouth is slightly open. Lips do not lean against incisors, protrusion
may develop. The tongue does not lean against the palate, the transversal growth of the upper jaw
from the median palatal suture stagnates, and the upper jaw is narrow showing the Gothic palate,
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resulting in cross bite. This is enhanced by the pressure of cheeks at open mouth and by the
insufficient ventilation of the nasal cavity.
Insufficient lip closure – When at rest, the upper and lower lips should be in contact, without the
muscle tension of circumoral muscles. Excessive muscle tension may lead to the retrusion of
frontal teeth. Members of some ethnic groups have very full but flaccid lips that create very small
force on the frontal teeth. The pressure of the tongue at the insufficient anti-force of lips causes the
protrusion of frontal teeth in both dental arches. Lip closure in some patients is not sufficient.
Causes include short lips, retrognathic (dorsal position) lower jaws, and enlarged lower facial third
or prominent upper incisors. Another type of the abnormal function of lips is pushing the lower lip
under the upper incisors, which leads to the protrusion of upper incisors and the retrusion of lower
incisors.
Early loss of temporary teeth – Temporary teeth are a natural spacer which keeps the space
necessary for the eruption of permanent teeth. Tooth crowding is a consequence of early loss.
Unilateral early losses with the non-aesthetic shift of the median line of the dental arch are
important.
Loss of a permanent tooth during the development – It causes the neighbouring teeth to decline
into the gap, results in the excessive eruption of teeth in the opposite jaw, reverse bite, and in the
shift of the median line of the dental arch, etc.
Injuries – Injury to a temporary tooth (usually to an incisor) may cause damage to the germ of the
permanent tooth, resulting in its deformation. According to the appearance of a deformed tooth,
various defects can be distinguished, for example angulation or dilaceration. Permanent teeth can
be lost as a result of injury. In children and adolescents, the fractures of the condylus of the lower
jaw are frequent which may lead to the asymmetric growth of the lower jaw and finally to facial
asymmetry. Post-traumatic solid scars may limit the growth of jaws by their pressure and deform
dental arches.
Hormonal effects – Growth hormone deficiency causes nanism, the patient has small jaws, with
significant crowding and the delayed eruption of teeth. In the case of acromegaly, which is caused
by the overproduction of the growth hormone, individual bones including the lower jaw are
enlarged as a result of excessive growth. Cretinism (thyroid hormone deficiency) is characterized
by the delayed eruption of teeth and the delayed growth of jaws, macroglossia.
Vitamin D deficiency (rickets) – deformation of jaws leads to the formation of the open bite.
7.3 Prevention and prophylaxis of orthodontic abnormalities
It is discussed in the previous chapter that the etiology of orthodontic abnormalities is
multifactorial and that the effect of inheritance is significant. The possibilities of prevention and
prophylaxis are therefore limited. The main aim of preventive measures is to ensure the proper and
harmonic development of the orofacial system and dentition whereas prophylactic measures focus
on the treatment of a particular abnormality. Preventive care during pregnancy is provided at
antenatal clinics to ensure the healthy development of the foetus. Mothers with a genetic load for
serious syndromes are subjected to genetic diagnostic tests. Postnatal prevention and prophylaxis
are ensured by a pediatrician and parents, later by a dentist or orthodontist.
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The positive effect of breast-feeding has already been mentioned. It is recommended that a child is
fed in irregular intervals according to his/her needs. In the case of artificial feeding, the conditions
as to the prevention of finger sucking should be similar to those at natural breast-feeding. During
feeding, the infant should be fully satiated and should also get tired. It is not therefore
recommended to shorten the period of feeding. An opening in the bottle teat should be big enough
to allow the milk to drop away when the bottle is turned upside down. During feeding, the child
should be in the vertical or slightly bevelled position, and the bottle should be placed horizontally.
The shape of a bottle teat is also important. Anatomically shaped dummies (NUK) that are
currently available on the market can simulate the natural anatomy during feeding. They help keep
the tongue in the natural position and force the infant to push his/her lower jaw forward.
The use of a dummy during the day is normal. During mental development, children get rid of their
bad habits spontaneously. If a child gets rid of this bad habit before the age of 3 or 4 years, possible
deviations in dental arches will be corrected and will not be carried over to the mixed and
permanent dentition. Some children develop mental dependence on sucking. Taking the dummy
from the child would be a major error. In such a case, the child will start to suck his/her finger
which will press on dental arches with greater force, causing major deviations. Weaning away from
dummy sucking is demanding and requires the cooperation of parents. The child should be
engaged in some activity during the day so that he/she will forget about his/her bad habit. The child
releases internal emotional tension through dummy sucking. This is why some children will not
fall asleep without dummy sucking. Weaning away must therefore proceed in a kind and peaceful
atmosphere. Parents should not rebuke their child. The child must understand that it is for his/her
good and it is not a punishment. In older children (at the pre-school age), a vestibular screen can be
used to replace the dummy as an aid to help wean away dummy sucking. A ready-made vestibular
screen is a plate made of flexible plastic. The child puts this screen into the vestibulum of the oral
cavity where he/she holds it by pressing lips together, which also strengthens the lip closure and
prevents mouth breathing. The pressure of the screen on the protruded incisors will correct their
position.
In children with persisting mouth breathing, it is necessary to ensure the passage of the upper
airways, and perform adenotomy, if necessary.
Muscle exercises (myotherapy) are supplementary to orthodontic treatment in children with flaccid
lips and insufficient lip closure. Blowing, whistling, holding a planar object (for example a coin)
between lips, or blowing cheeks is recommended.
From a preventive and prophylactic point of view, the early loss of temporary teeth can be
prevented. Care should focus on the prevention of dental caries (fluoridation, healthy diet, regular
and thorough oral hygiene) and on the early treatment of temporary teeth. Temporary teeth and
their roots destructed by persisting caries may deflect erupting permanent teeth from their natural
position. The early extraction of such teeth is therefore necessary. If a temporary tooth is lost early,
the orthodontist must decide on whether or not it is suitable to use a spacer.
Some children do not show natural abrasion (wear) of temporary teeth. Non-abraded temporary
canines or temporary incisors (less frequently) force the lower jaw to forced bite. This means that
at the full bite into the position of maximum intercuspidation, the lower jaw must be pushed
forward to reverse bite or deflect aside to cross-bite. At forced bite, the head of the jaw joint is in
the unnatural (usually asymmetric) position which leads to the asymmetric growth of the lower jaw.
Such cases require the selective shaping of temporary teeth to establish natural articulation
conditions.
The Milwaukee corset used to treat spinal scoliosis can negatively affect the development and
growth of the face and teeth. With its cranial pressure on the lower jaw, it causes the shortening of
the lower third of the face, deep bite, protrusion and the fan-like divergence of upper incisors. In
order to prevent such adverse effects, orthodontic apparatus is indicated to stabilize the dentition.
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8. DISEASES OF JAW BONES____________________________________________________
8.1 Osteopathy
8.1.1 Polyostotic osteopathy
Diseases of the bone system are generally covered under the term of polyostotic osteopathies
which have different etiologies and manifest themselves by disorders in bone structure and density.
From an etiological point of view, osteopathies can be divided into developmental and acquired
(metabolic, endocrine, vascular) osteopathies. Monoostotic osteopathies are disorders that only
affect jaw bones.
According to pathogenesis, they can be divided into the following forms:
–
osteoporosis (atrophy)
–
osteosclerosis
–
–
osteomalacia
fibro-osteoclasia
declining bone mass (the atrophy of the gingival process after
the loss of teeth – it deteriorates retention conditions in dental
removable replacements)
the growth of bone mass (exostoses: torus palatinus, torus
mandibularis)
a disorder of bone mineralization
the extreme reconstruction of a bone
8.1.2 Monoostotic osteodysplasia of jaws
Besides its mechanical function, the bone also ensures calcium homeostasis, contributes to
acidobasic balance, and creates the space for bone marrow. Good balance in the complicated
coordination of activities of bone cells (osteoblasts, osteoclasts and osteocytes) is responsible for
the growth of bones, bone remodelling and regular bone restoration. The complexity of
pathological changes becomes even greater in the jaws due to the teeth, their development and
modification. Disorders of these activities bring about changes in full-value bone tissue which can
be divided into diagnostic categories with respect to the predominant bone disorder.
8.2 Disorders of the maturation of bone mass components
Fibrous osteodysplasia
The nature of this disease lies in the conversion of bone marrow into fibrous tissue with a different
degree of the capacity of cartilaginous or bone metaplasia. It is a disorder of differentiation of
mesenchyme and has many synonyms, for example dysfibroplasia (Edlinger), fibrous
osteodysplasia, ostitis fibrosa, ossifying fibroma, osteofibroma, Jaffé-Lichtenstein disease,
Uehlinger disease. Familial fibrous dysplasia with typical hypertelorism is called cherubism. It can
be caused by hormonal deviations (pubertas praecox) or possibly by some chemicals whose
harmful effect cannot be excluded. Reaction comes out of the marrow and leads to the gradual
reconstruction of the corticalis and spongiosis and finally to the deformation of the outer shape of
the bone. In the case of the congenital form, the deviation in the mesenchyme causes tissue
metaplasia resulting in atypical fibrous bone, the imbalance between osteoblasts and osteoclasts,
and disturbed mineral exchange.
(The origin of the disease is likely to be associated with the interruption of bone tissue maturation
which may result from the defective embryonic development of bones).
The microscopic finding is characterized by the presence of cell fibrous tissue consisting of
spindle-shaped fibroblasts and myofibroblasts, with the aggregates of collagen fibrils among them.
However, in some cases it is not practically possible to identify the type of a skeletal disease only
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on the basis of a histological finding or only on the basis of a clinical finding, and one should also
look at the dynamics of the development of clinical and X-ray findings. It is therefore necessary to
repeat bone excision with the increasing age of a patient.
The disease that has affected the facial skeleton results in facial deformations and disorders of the
dentition of a different degree. The disease is usually benign and progresses slowly. It may develop
for years. The disease is not inherited; women suffer from this disease more often than men. The
disease usually begins in childhood, showing a progressive development up to puberty and
becoming inactive after the termination of the skeletal development. Malignant transformations of
fibrous dysplasia in the craniofacial region are very rare.
8.3 Disorders of bone tissue caused by hormonal dysfunction
Osteodystrophia fibrosa (cystica) generalisata (Recklinghausen’s disease), primary
hyperparathyroidism
In most cases, this disease is caused by the overproduction of parathyroid hormone which results in
the reduced absorption of phosphates in renal tubules which leads to hypercalciuria (stones,
secondary uremia, hypercalcemia). The same conditions occur after long-term hemodialysis.
Bones show the isolated spots of demineralization, the multiplication of osteoclasts which look as
giant, multinuclear cells with the progressive degradation of bone, spreading from the inside of the
bone through Haversian canals up to the corticalis. These conditions are difficult to distinguish
from giant-cell granuloma (histological findings are the same). These disorders can also be
monostotic and localized in the jaw. The overproduction of somatotropin growth hormone (STH)
causes acromegaly – the enlargement of the lower jaw.
8.4 Diseases of bone tissue caused by metabolic disorders
Rickets
Disorders of vitamin D absorption lead to the increased activity of osteoblasts, accompanied with
the increased level of alkaline phosphatase. Mineralization is insufficient, which can be observed
particularly at the border between the bone and cartilage; there are also disorders of the tooth
mineralization, the eruption of teeth is delayed, osteomalacia may occur in adult patients.
8.5 Disorders of bone tissue formation caused by unknown factors
Paget’s disease – osteodystrophia deformans
Causes are still unknown. According to some theories, it is caused by paramyxoviruses, which
would confirm the original hypothesis by J. Paget, who described this disease in 1877 as the
chronic inflammation of bone tissue. The disease manifests itself at older age (after the age of 50
years). Damage to the scull occurs at the base and calva; jaws are rarely damaged. The disease has
three stages, with bone thickening and obvious sclerotization in the last stage.
The histological finding shows the predominance of osteoclasts with typical lacunae in the
compacta and on spongiotic trabeculae. Haversian canals are excessively supplied with blood and
enlarged. In the developed stage, differences between the compacta and spongiosis disappear. The
bone consists of rough trabecular structure with partial calcification. Bone marrow is largely
replaced with cell fibrous tissue and collagen fibrils. Teeth show hypercementosis on the roots.
From an oncological point of view, the Paget’s disease is preblastomatosis; 5-20% of its advanced
forms may become malignant.
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Major clinical symptoms include pain or the intensifying of the existing pain, the intumescence of
bones covered by the skin; pathological fractures may also occur relatively frequently.
8.6 Necroses and inflammations of jaws
8.6.1 Bacterial
Osteomyelitis (Osteomyelitis acuta)
It is the acute or chronic inflammation of bone marrow which is usually induced by pyogenic flora.
The most common causes of the inflammation of odontogenic origin include apical periodontitis,
cystogranuloma or purulent radicular cyst which is associated with the inflammatory reaction in
bone marrow, Haversian canals (the embolism of the vessel) and the gradual spread of infection in
the periosteum whereas the mineralized bone reacts only passively. Although such inflammatory
foci frequently occur in jaws, osteomyelitis is currently a very rare disease. The transmission of
osteomyelitis via blood is extremely rare; pathogens include haemolytic Staphylococcus sp.
In infants, the inflammation spreads from the medium ear, affecting mainly the upper jaw. In adults,
the lower jaw is affected in most cases. Osteomyelitis sicca is currently the well-known and quite
common form of osteomyelitis that occurs chronically without apparent purulence. Osteomyelitis
is often latent, manifesting itself by blunt pain in the jaw and the Vincent’s symptom (paraesthesia
in the region of the mental nerve (nervus mentalis)).
Treatment is based on the long-term application of high doses of antibiotics sensitive to the
particular infectious agent; cultivation tests are also performed during treatment. Surgical treatment
focuses on the incision of abscesses formed in soft tissue; after lifting the periosteum, the
trepanning of the superficial compacta is performed followed by the removal of bone sequesters
and the fixation of loose teeth. Treatment in hyperbaric// chamber is also recommended.
8.6.2 After irradiation
Osteoradionecrosis
The exposure of jaw bones to radiation during the treatment of malignant tumours in the oral cavity,
hypopharyngus or jaws may cause serious damage due to the elimination of osteocytes and
osteoblasts; the fibrotization of bone marrow occurs and vessels supplying the periosteum may also
be damaged.
In the beginning, such damage is not visible and may remain latent for years. Unlike purulent
osteomyelitis, no reactive processes in the periosteum accompanied with the new formation of
bone are observed. Infection may usually enter the poorly supplied bone via an open wound after
tooth extraction, or from inflammatory processes in the jaw or from decubitus caused by removable
dental replacement. It is caused by more factors. Causal therapy is difficult. Infection causes bone
necrosis; the dead parts of bone must be removed by resection.
8.6.3 Prevention of osteoradionecrosis
As part of prevention prior to radiation, it is necessary to eliminate all potential causes of
inflammatory irritation and perform the radical extraction of teeth. Consultation with the informed
dentist is also necessary prior to treatment. If the extraction of teeth has to be performed later, it
should be carried out under the antibiotic screen and should be followed by a specialist.
8.6.4 Chemical (drug-induced)
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Bisphosphonate-induced osteonecrosis
Bisphosphonates are part of the comprehensive therapeutic strategy in patients who have bone
metastases, or suffer from disorders of bone metabolism such as osteoporosis. The effect of
biphosphonates is based on their selective uptake in bones where they create a protective barrier
against bone destruction. They inhibit bone cells – osteoclasts - by interfering with the metabolism
of triphosphates and have a significant anti-angiogenic effect that provides a desirable anti-cancer
action.
After the first introduction of bisphosphonates in therapy, effects such as the impaired quality of
bone tissue in jaws were not observed. Since 2004 we have treated patients who showed
complications such as alveolitis and the spread of necrosis after tooth extraction (mostly in the
lower jaw) after long-term bisphosphonate therapy. The nature of these complications lies in the
impaired vascularization of bone tissue which is associated with the presence of nitrogen atoms in
modern bisphosphonates. Initial symptoms such as very intense pain were alleviated by
conservative therapy. However, healing was not observed and some patients developed major
ostitis and osteomyelitis. The necrotic, decaying bone must be treated surgically, using
sequestrectomy and the partial resection of the bone without affecting the integrity of the jaw. The
course of post-extraction complications is similar to that known in jaws with osteodionecrosis after
radiotherapy. Osteonecrosis is often observed in patients treated for multiple myeloma, breast, lung
or prostate carcinoma. These complications sporadically occur in patients with osteoporosis.
Prevention of the osteonecrosis of the jaw after bisphosphonate therapy
When preparing a plan of treatment, the dentist must identify, perceive and correctly assess
potential complications associated with therapy. As with the treatment of the irradiated jaw, the
dentist must also be fully informed before initiating the treatment of patients with long-term,
bisphosphonate therapy and performing the early preventive extraction of teeth. When planning
surgical treatment, the dentist must ensure sufficient antibiotic therapy in a patient, reduce
vasoconstrictive effects of local anaesthetics during extraction to a minimum, treat the wound after
extraction thoroughly, and protect blood coagulum formed in the extraction wound. If
complications occur, he/she must initiate immediate effective long-term antibiotic therapy
supported by surgical interventions in order to remove necrotic and non-regenerating bone.
The main objective is to create interdisciplinary cooperation in order to give the patient a specialist
dental examination prior to treatment, and design a plan of treatments that includes the prevention
of possible problems and the consistent standard treatment of all identified dental and jaw
pathological conditions. Patients with the above-mentioned complications should be referred to
specialized clinics.
8.7 Bone cysts
Odontogenic cysts are most common bone cysts in jaws. Radicular cysts are among most common
cysts followed by developmental follicular cysts and rather rare periodontal cysts.
The original cyst has an epithelial lining in the preformed bone cavity and is usually filled with
liquid or solid mass. Its formation requires the presence of epithelium that is chronically irritated,
for example by inflammation. With its activity, it forms small cavities which gradually combine to
form a large cavity. The cyst wall consists of a semi-permeable membrane that regulates the
osmotic conditions in the cavity. With the increasing influx of body fluids into the cyst, the cyst
will expand which will result in the resorption of the surrounding bones and cyst enlargement.
This behaviour is typical of radicular cyst where the epithelial residues of the dental lamina are
permanently irritated by the non-vital tooth which leads to the growth of the cyst that may severely
destruct the jaw. The same applies to the growing developmental cyst adjacent to a submerged
tooth that has not yet erupted. Treatment of such bone cysts requires the removal of the epithelial
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lining of the cavity and the elimination of all potential causes of repeated irritation of possible
epithelial residues.
Other bone cysts in jaws not related to teeth also grow in locations with epithelium residues, bone
fissures and embryonic ducts (ductus thyreoglossus, palatal cysts, etc.).
The bone pseudocyst has no epithelium in the cavity. Its formation is associated with changes in
the blood or lymphatic basin, injuries and other causes.
8.8 Bone tumours
Benign tumours localized in the jaw bone are usually mesenchymal tumours such as fibroma,
osteoma, chondroma, hemangioma, and lymphoma. Their composition may combine all these
types of tissues. Due to their location, they may pose a serious risk (for example, central
hemangioma in the jaw after tooth extraction may cause major bleeding). Odontogenic tumours are
also located in jaws; ameloblastoma growing from epithelial tissue is most common followed by
rather rare dentinoma and cementoma.
Most common malignant tumours include fibrosarcoma, malignant fibrous histiocytoma. Epithelial
tumours include carcinoma growing from the surrounding or metastases of a distant tumour. Apart
from fibrosarcoma and histiocytosis, the Ewing’s sarcoma is the most common malignant bone
tumour in children.
9. PREPROSTHETIC SURGERY OF EDENTULOUS JAWS __________________________
Preprosthetic surgery corrects the unfavourable relations of alveolar processes after tooth
extraction, the use of unsatisfactory or unstable total dentures that may cause the atrophy of the
alveolar bone or changes in soft tissue around the jaws.
The main aim of preprosthetic surgery is to create the optimum prosthetic bed. The successful
outcome of a surgical intervention depends on the early indication for surgery (one should not wait
until the atrophy of bone tissue deteriorates), the suitably chosen type of preprosthetic modification,
exact surgery, thorough postoperative care and perfect prosthetic treatment.
The atrophy of the alveolar process of the jaws can be divided into six classes according to the
Cawood’s scale: starting from the condition immediately after tooth extraction without any
significant atrophy to the excessive atrophy of bone tissue in the upper and lower jaws.
Preoperative evaluation is based on the following items:
– the assessment of the OPG of the jaws which reveals the extent of bone tissue atrophy,
– the clinical examination of the prosthetic bed and the assessment of the condition of soft and
hard tissues of jaws,
– the patient’s general condition – the assessment of general diseases,
– the patient’s financial capacity – the selection of augmentation based on biocompatible
materials or the introduction of dental implants,
– the assessment of the patient’s mental state and his/her ability to cooperate with the physician
in the postoperative period.
The patient’s age may not be necessarily a limiting factor.
9.1 Preprosthetic corrections of alveolar processes of jaws
Partial preprosthetic corrections of hard and soft tissues without apparent jaw atrophy.
The elevation of atrophic alveolar processes.
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a) Relative elevation of the alveolar process – the reconstruction of soft tissues around the jaw;
b) Absolute elevation of the alveolar process – osteoplastic surgeries
Implantation procedures
a) The augmentation using biocompatible materials
b) Dental implants
Segmental distraction osteogenesis.
9.1.1 Partial preprosthetic corrections of alveolar processes without apparent bone tissue
atrophy
Alveoloplasty (egalization) is used to correct the unevenness of the alveolar bone, undercuts, the
protrusion of the alveolus, exostoses such as torus palatinus and mandibularis.
All these types of unevenness and formations would lead to the instability of the total denture and
decubitus.
Partial corrections of soft tissues are performed to remove folds and frenula that would release the
dentures – labial and lingual frenulectomy, the extension of buccal folds.
The excision of the fibrous hypertrophy of maxillary tubers, granuloma fissuratum (a fibrous
formation in the vestibulum caused by the movement of unstable dentures). Excision is perform to
restore the optimum prosthetic bed in order to eliminate the chronic irritation of the formation and
its potential malignancy.
9.1.2 Elevation of atrophic alveolar processes
9.1.2.1 Relative elevation of the alveolar process
This kind of surgery is indicated in the case of unserious atrophies of the alveolus in the upper jaw
or in the lower jaw at the shallow vestibule in the absence of the apparent alveolar atrophy.
Plain vestibuloplasty is a simple procedure. Its principle relies in the supraperiosteal preparation of
the mucous vestibular flap and its fixation using absorbable suture in the newly created vestibular
vault. The exposed periosteum will heal per granulationem. Immediately after surgery, it is covered
with covering plate Erkopress with repine bandage.
In the lower jaw, the plastic reconstruction of the vestibule and the oral base according to Trauner
and Obwegesser is preferred, with covering the periosteum using a free skin graft collected from
the skin on the thigh. The fixation of the skin graft is ensured by a carrier with circummandibular
fixation for a period of one week. This surgery is demanding with regard to the patient but provides
a very good outcome.
Postoperative dentures are made in 7-14 days for 3-4 months.
9.1.2.2 Absolute elevation of the alveolar process
Elevation was based on the use of bone grafts (from the hip or rib). Surgeries were performed in
the 1960ies and 1970ies. A number of demanding surgical procedures were developed. Bone grafts
loaded by the prosthesis show more than 50% resorption in 2-3 years. As a result, the effect of
surgery was largely lost.
Osteoplastic surgeries of this kind were replaced by implantation procedures.
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9.1.3 Implantation procedures
9.1.3.1 The augmentation of atrophic jaws using biocompatible materials derived from
hydroxyl apatite, tricalcium phosphate and bio-glass.
These techniques showed a boom in the 1980ies along with the development of respective
materials. Their main advantage is that they do not resorb and show good resistance against
chewing pressure. They are placed subperiosteal to the apex of the alveolar process of the atrophic
jaws and heal in for 2 – 3 months. After augmentation and healing, the upper jaw will require
vestibuloplasty whereas the lower jaw will require the Trauner-Obwegeser reconstruction of the
vestibule and the oral base. The outcome of such surgeries is very good. However, augmentation is
not indicated in severe atrophies of jaws (pencil-thin mandible).
9.1.3.2 Implantation procedures – enosseal dental implants.
This topic is discussed in other chapter.
9.1.4 Segmental distraction osteogenesis
Modern techniques are used to address the advanced resorption or post-traumatic bone loss.
Distraction osteogenesis is a biological process to form new bone tissue between the distracted
segments.
Distraction force acts not only on bone tissue but also on the surrounding tissues by some tension
which leads to adaptive changes resulting in histogenesis. Distraction is based on a direct effect
between mechanical tension acting on osteoblasts and controlling growth factors (transforming
growth factor beta 1, insulin growth factor I.). This process mainly depends on vascularization, i.e.
the sufficient formation of the vascular supply to the regenerated bone tissue.
The surgical procedure is based on two vertical osteotomies connected by horizontal osteotomy
where the segment must not undergo slitting the lingual periosteum. A distractor is then attached
using screws to the jaw base and segment. The distractor is activated by rotation by 0.5 mm per
day. New bone tissue is formed between fragments.
After the revascularization and partial mineralization of new bone, dental implants can be placed in
the distracted segment in two months.
Segmental osteogenesis using distraction techniques is an efficient procedure for the preprosthetic
treatment of posttraumatic bone loss in the alveolar process in the frontal segment of the lower jaw,
the atrophies of the lower jaw in the distal segment where the introduction of dental implants is
planned in the second phase.
10. JAW ABNORMALITIES______________________________________________________
10.1 Etiology and classification of jaw abnormalities
Most jaw abnormalities show polygenic inheritance. Apart from inheritance, there are also internal
and external factors that contribute to the development of jaw abnormalities. They can affect the
development of the face and jaws not only in the intrauterine stage but also in the postnatal
development. A defect in the development that occurs before embryogenesis will result in severe
malformations such as dysplasia. Teratogenic factors acting in the period of the foetal development
may cause changes in the shape and size of jaws. Similarly, pathological factors in the postnatal
period will cause abnormalities such as hyperplasia or hypoplasia. Endogenic causes of jaw
abnormalities include: genetic predisposition, endocrine disorders (pituitary gland, thyroid gland),
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metabolic disorders (vitamin D). External conditions affect the neuromuscular component of the
face which contributes to the formation of facial bones. Such external factors include various bad
habits (finger sucking) and parafunctions, disorders in nose breathing, the early loss of teeth. The
growth zones of jaws can be damaged due to injuries, exposure to radiation. Such damage may
result in hypoplasia of a different extent.
The developmental disorder localized in the dentoalveolar region will result in deviations in the
position of individual teeth. The altered position of jaws (compared to the position of the scull
base) will manifest itself by the impaired jaw relation.
The basic classification of abnormalities is based on the mutual occlusal position of jaws (Angle
classes) – in completely dentate dental arches, the jaw relationship at the maximum
intercuspidation is determined by the position of canines and first molars.
a) Normal occlusal relationship (Angle Class I) – The interbuccal tubercle of the upper first molar
fits into the inter-tubercle groove of the first lower molar while the apex of the upper canine fits
between the lower canine and the first lower premolar.
b) Distal occlusion (Angle Class II) – the distal position of the lower molar and canine against
antagonists; prognathism, microgenia, maxillary prognathism.
c) Mesial occlusion (Angle Class III) – the mesial position of the lower molar and canine;
progenism, retrognathism, micrognathism, mandibular prognathism.
The deviation located in the vertical plane results in open bite or deep bite. The asymmetric growth
of the lower jaw results in laterognathism manifested by lateral asymmetry in the region of the
lower facial third.
Different morphological deviations called syndromes may occur in the orofacial region. Individual
facial syndromes are characterized by a group of symptoms that describes a particular abnormality
caused by a disorder in the development of the face. Defects occur in the development of teeth,
jaws and facial soft tissue. Hemifacial microsomia is the most common facial syndrome being
characterized by the unilateral hypoplasia of the face of a different extent. The insufficient
development is manifested most significantly in the region of the branch of the mandible and the
jaw joint. Depending on a degree of a particular disorder, the deformation or agenesis of the auricle
can be present.
10.2 Patient examination
10.2.1 Examination of the patient’s general state of health
The patient scheduled for a corrective surgery must undergo tests to determine his/her general state
of health including the psychological evaluation of the patient's personality that is also very
important. It should be emphasized that a jaw abnormality does not pose a risk to the patient’s
health. The surgery is not therefore recommended in patients in whom it would be risky because of
the patient’s general state of health. For example, this applies to patients suffering from a blood
coagulation disorder, serious cardiovascular disease, etc. In patients with the history of a mental
disease it is necessary to obtain an opinion of their psychiatrist. At a disproportionately high risk
associated with a particular surgical treatment, orthodontic correction is indicated although the
outcome may not be perfect. This decision has to be made on the basis of the patient’s recorded
history at the very first consultation of the therapeutic plan.
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10.2.3 Examination of the orofacial system
The examination of the orofacial system must include the complete assessment of the face, the
determination facial characteristics and the identification of a deviation caused by the anomalous
position of the jaws. The main goal of therapy is to achieve not only normal occlusal relationship
but also the well-balanced harmonic appearance of the face. The extraoral and intraoral
examination is performed to establish the diagnosis and choose the type of a corrective surgery.
Additional examinations include the analysis of jaw contours and the analysis of the patient’s
teleroentgenogram, i.e. the distant X-ray image of the scull and facial profile. The analysis of
craniometric angles and points in the teleroentgenogram provides detailed information on the exact
extent of the abnormality; it particularly determines the jaw relation towards the scull base.
10.3 Treatment of jaw abnormalities
Reasons of the surgical treatment of jaw abnormalities can be aesthetic and functional and also
psychological. In most case, it includes comprehensive orthodontic and surgical therapy. As
required by the surgeon, the orthodontist will perform the orthodontic pre-treatment of dental
arches using fixed apparatus in order to achieve the regular configuration of teeth and regular
arches which will match in the new planned configuration of normal occlusion.
Using the models of jaws, the planned shifts of jaws will be simulated in order to clarify the
requirement concerning orthodontic pre-treatment.
Orthodontic preparation will take 2-3 years on average. Corrective surgery is performed when the
growth of one or both jaws is completed (usually at the age of 16-18 years). During bone healing,
which lasts 6-8 weeks, the patient will receive mushy food, followed by orthodontic after-therapy
and a retention period of 2 years, in most cases.
The main goal of corrective surgery is to shift the maxilla, mandible or both jaws to the new,
planned, normal occlusal relationship. This shift must be in accordance with the general
appearance of the face in order to improve both the function of the dentition and the aesthetic
appearance of the face.
There are many kinds of osteotomies. However, the majority of jaw abnormalities can be corrected
using Le fort I line osteotomy in the upper jaw or using the sagittal osteotomy of the mandibular
branches. These methods constitute basic corrective procedures of orthognathic surgery.
10.3.1 Le Fort I line maxillectomy:
The principle of the surgery is to separate the lower third of the maxilla. Osteotomy is performed
through the bottom of the jaw cavity and the bottom of the nasal cavity, and through the tuber of
the maxilla in the distal part. The nasal septum is interrupted at the bottom of the nasal cavity and
the tuber of the maxilla is separated from the pterygoid processes. After osteotomy, the lower third
of the maxilla is released – the alveolar process with the palate and this part is then shifted as
planned.
1.3.2 Sagittal osteotomy of mandibular branches:
It is based on the split of the branch of the lower jaw. Bilateral split allows the body of the lower
jaw together with the medial sheet of the branch to be shifted mesially and distally. The lateral
sheet of the mandibular branch, which forms a unit with the joint process, will remain on place.
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After achieving the normal occlusal relationship, the branch is firmly fixed using screws or bone
splints.
10.4 Individual types of jaw abnormalities
10.4.1 Class II jaw abnormalities
Apart from definitions based on the relationship between upper and lower canines and molars,
Class II jaw abnormalities are characterized by the positive incisal step, i.e. the gap of a different
size between upper and lower incisors in the sagittal plane – “overjet“. This condition arises due to
the enlargement of the maxilla or due to the hypoplasia and distal position of the mandible. This
includes:
Maxillary prognathism (prognathia maxillaris) – the excessive growth of the maxilla usually in a
forward direction, the protrusion of upper frontal teeth.
Microgenia – the lower jaw is small, insufficiently developed, in the distal occlusal configuration,
the protrusion of lower frontal teeth, the hypoplasia of the mental protuberance.
Retrognathism – the mandibula is normally developed, being in the distal position relative to both
the maxilla and the scull base. A characteristic feature is that the mandibular angle (i.e. the angle
between the branch and the body of the lower jaw) is reduced.
Therapy: orthodontic pre-treatment is followed by corrective surgery – bilateral sagittal osteotomy
of mandibular branches and the anterior shift of the mandible into the normal occlusion
configuration.
10.4.2 Class III jaw abnormalities
include a prognathic kind of abnormalities characterized by mesial occlusion and negative incisal
step – “reverse bite”. This condition arises due to the insufficient growth of the maxilla, the
retroposition of the maxilla, or the hyperplasia of the mandible, particularly in the sagittal direction.
Micrognathism – the maxilla is hypoplastic, all dimensions are usually reduced compared to the
normally developed mandible.
Retrognathism – the upper jaw has more or less normal dimensions with regard to the remaining
parts of the facial skeleton but it is in the distal position relative to the scull base and the normal
configuration of the mandible.
Progenism – it is usually characterized by the enlargement of the mandible, particularly in the
sagittal plane, with the prominent chin in the facial profile.
Therapy: Orthodontic pre-treatment using fixed appliances followed by corrective surgery. In the
case of progenism, the bilateral sagittal osteotomy of mandibular branches and distal shift is
usually performed. In the case of micrognathism and retrognathism, the configuration of the
maxilla is corrected by means of Le Fort I line maxillotomy with the anterior shift. Osteotomy of
the maxilla can be used to correct some cases of minor progenism, it depends on the general
appearance of the face and its character. Major progenism is corrected by bimaxillary surgery –
based on the anterior shift of the maxilla after Lf I line maxillectomy and the bilateral sagittal
osteotomy of mandibular branches with the distal shift into the normal occlusal relationship.
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10.4.3 Jaw abnormality in the vertical and horizontal planes
Open bite (mordex apertus) – this malocclusion occurs in the vertical plane; a gap of a different
extent is formed in the frontal segment of the dentition so that only teeth in the lateral part
articulate. This abnormality is called “open bit”. It is characterized by the extension of the lower
third of the face.
Therapy: Orthodontic pre-treatment and the Le fort I line osteotomy of the maxilla, with excision
and impaction of the distal part of the upper jaw. The sagittal osteotomy of mandibular branches
are necessary relatively frequently in order to achieve a proper mutual configuration in the sagittal
plane.
Laterognathism – this abnormality is caused by the asymmetric growth of one half of the mandible.
Most cases are characterized by the hyperplasia of one side of the mandible which is usually
localized in the joint process. The abnormality is manifested by cross bite (with regard to
occlusion) and by asymmetry in the region of the mental protuberance shifted to the smaller side
(outwardly).
Therapy: Orthodontic pre-treatment followed by corrective surgery on the mandible – the bilateral
osteotomy of mandibular branches. The lower jaw is rotated in the horizontal plane to the normal
occlusal configuration relative to the upper jaw.
10.4.4 Post-cleft and post-traumatic deformities
The surgical treatment of cleft abnormalities may result in defects in the growth of the maxilla
caused by existing surgical wounds that prevent normal development of the jaw. This results in
pseudoprogenism associated with cleft treatment which is characterized by reverse bite and
hypoplasia of the maxilla. Unilateral cleft is manifested by lateral asymmetry of the maxilla.
Correction is performed by means of the Le fort I line osteotomy of the maxilla, usually combined
with the sagittal osteotomy of mandibular branches.
If growth centres of jaws (particularly in the region of joint processes) have been damaged as a
result of injuries in childhood, the normal growth of jaws may be affected, causing posttraumatic
abnormality. A posttraumatic abnormality can also be caused by the untreated or poorly treated
fracture of jaws.
Therapy of such conditions is similar to those of congenital abnormalities.
11. BIOLOGICAL AND BIOPHYSICAL ASPECTS OF ORAL IMPLANTOLOGY _______
Current implants are usually made of titanium (Ti), or less frequently of zirconium (Zr), tantalum
(Ta), and niobium (Nb). Another technology is based on the application of a single or multiple
layers (coating) on the core made of a particular metal alloy (for example on the surface of
hydroxyl apatite, zirconium nitride etc.). The rate and amount of released ions is also an important
characteristic of a material. The release of ions can be significantly reduced by the proper selection
of the type of surface treatment or by the application of layers on a particular core. This is
advantageous with regard to compatibility.
11.1 Biological properties
Materials can be divided according to their biological properties (biocompatibility) and mechanical
and physical properties. On the basis of biological properties, materials can be divided as follows:
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11.1.1 Biotolerant materials
– heal in the bone by fibrointegration. This means that there is an interlayer of soft tissue being
formed between the implant and bone, allowing the implant to heal in. From an implantological
point of view, this kind of healing is undesirable.
11.1.2 Bioinert materials
– heal in the bone by osseointegration. No interlayer is formed between the implant and the bone.
The implant is closely attached to the bone without any obvious bond between the implant and
bone. This kind of healing is ideal from an implantological point of view.
11.1.3 Bioactive materials
– heal in the bone by biointegration. It is likely that a bond is formed between the implant and
bone tissue during the healing of implant. This kind of healing is the most suitable in implantology.
11.2 Mechanical and physical properties
On the basis of mechanical and physical properties (thereinafter marked as m-p properties) (see
Table 1), materials can be divided as follows:
11.2.1 Materials with excellent m-p properties
– These materials show very high resistance.
They are therefore most suitable from a mechanical point of view. However, they are less suitable
with respect to corrosion and the least suitable with regard to biological properties.
11.2.2 Materials with satisfactory m-p properties
– Compared to the above-mentioned materials, these materials have worse m-p properties but have
a wide range of applications in oral implantology.
11.2.3 Materials with poor m-p properties
– These materials that have the worst m-p properties usually belong to a group of bioactive
materials. Thanks to their biological properties, they are on the highest place in the assessment
scale.
Coating is another possibility of making a material with good m-p as well as biological properties
and preserve biocompatibility. The core consisting of the material with good mechanical and
physical properties is coated using a very thin layer (nanometres to micrometres) of another
material such as zirconium nitride, titanium nitride, hydroxyl apatite, etc.
Table 1
Comparison of biological and mechanical and physical properties of materials used in
implantology
Biological properties
Biotolerant
Bioinert
Type of material
Mechanical and physical
properties
Best, mechanically resistant
Alloys of precious metals
Alloys of general metals
Cr-Co-Mo alloys
Titanium and its alloys
Ta, Nb
Zr and zirconiumoxide ceramics
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Good mechanical properties,
sufficient for the use in oral
implantology
Worse properties
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Bioactive properties
Tricalcium and tetracalcium
ceramics, hydroxyl apatite ceramics
The worst mechanical properties in
the entire scale
11.3 The use of dental implants in other indications
Dental implants and their specific variations can also be used in non-dental indications. Such
indications can be divided according to the field, in which they are used, and include orthodontics,
plastic surgery, maxillofacial surgery and last but not least periodontology.
In orthodontics, dental implants are used for the shifting (medial or distal) of teeth. In such cases
and also in typical dental indications, they serve for the straightening and shifting of teeth,
anchoring implants. These implants have currently become standard part of orthodontic treatment.
Conventional dental implants in orthodontics are used to treat hypodontia, i.e. the condition
characterized by a small or large decrease in the number of permanent teeth where anatomic
conditions and articulation of the oral cavity allow the place to be made for the introduction of
dental implant. The rate of this type of hypodontia is currently on the rise. Typical examples of
hypodontia include missing lateral upper incisors, lower or upper second premolars, or the missing
canine or the retention of the canine without the possibility of its introduction into the dental arch.
Most serious cases of hypodontia may include total anodontia where no permanent tooth is
submerged. This is a serious defect accompanied with the atrophy of the alveolus that is not
suitable for further treatment using implants.
Plastic surgery uses special implants that are applied in loss locations, including epitheses after
major surgeries due to tumours. The implant forms a reliable anchor system for the replacement of
the lost tissue. Another possibility is to use fixation screws in combination with bone grafts.
In maxillofacial surgery, implants are used to anchor the miniplate that is part of the systems used
to treat the fractures of jaws and facial bones. They include splints that are fixed using self-drilling
screws which are basically implants. Another possibility is to use fixation implants to transfer
tissues, bone grafts to a different region. Self-drilling fixation screws are used to achieve the
perfect adaptation of transferred graft.
In periodontics, implants are used in indications to cover biomaterials with help of titanium nets or
special reinforced membranes. Self-drilling small implants are used to fix a particular membrane or
net.
Mini-implants form a special group of implants that are used in dental indications in cases of early
load. They are used mainly for the immediate attachment of removable dentures where
implantation after extractions is not possible for various reasons. However, these implants are only
temporary. There are distinct features of mini-implants and the narrowest two-phase implants that
the term “temporariness” is rather obscure as this kind of implants can be used in conventional
indications as definitive treatment.
11.4 Augmentation – replacement, tissue restoration
Augmentation techniques used in dentistry can be closed (1) or open (2).
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11.4.1 Augmentation methods
1. Closed augmentation techniques include the sinuslift surgery, which is the internal filling of the
jaw cavity with biomaterial, or biomaterial combined with bone. Two methods to perform the
sinuslift are available. The first one-phase method is based on the introduction of the implant and
biomaterial at the same time. The main prerequisite for this type of implant introduction is that
there must be a sufficient amount of bone horizontally, i.e. at least 4 mm (or 3 mm for the splinting
of implants). In the second two-phase method, augmentation is performed first followed by
implantation in 6–12 months.
2. Open techniques include the transfer of augmentation material to the place of augmentation.
Basically, it is the augmentation of the alveolar bone in cases of a relative or absolute deficit where
augmentation proceeds as bone building.
11.4.2 Augmentation material
Augmentation material can be autogenous and allogeneic. Autogenous material consists of a bone
transplant which was transferred from a certain region to a particular region as required. This
material has ideal biological properties. Allogeneic materials are based on hydroxyl apatite, betatricalcium phosphate, coral, bovine bone or glass-ceramics and can be combined with a plate
growth factor. Membranes used to cover biomaterials in periodontics can be resorbable or nonresorbable. Either membrane has specific predefined indications.
12. GENETIC ASPECTS OF DISEASES IN THE CRANIOFACIAL REGION ___________
Diseases of the craniofacial region may cause severe discomfort and stress in a patient since they
can be associated with major cosmetic problems that are perceived individually. This kind of
diseases is usually treated by plastic surgeons or dentists. The role of genetic consulting concerning
potential recurrence is very important in the diagnostic process.
12.1 Orthodontic abnormalities
Inheritance is a major factor in the development of orthodontic abnormalities. The role of genetic
factors in the formation and development of orthodontic abnormalities is seen particularly in the
familial incidence of some dental irregularities (for example mandibular progenism in the House of
Habsburg observed in many generations throughout the centuries) and the studies in twins (the rate
of some abnormalities in monozygotic twins is higher than that in dizygotic twins).
In spite of expectations that the inherited abnormalities of the dentition and jaws will manifest
themselves mostly in the temporary dentition, a great number of inherited irregularities can be
found, showing their symptoms in the permanent dentition at puberty. Within variability in the
development of the orofacial system, it can be concluded that inheritance determines parameters
such as the size and shape of the jaws, the period and manner of the growth of jaws, the size, shape
and number of teeth including the position of dental germs, and the time of tooth eruption. In
addition, individual traits can be mutually independent (the child can inherit small jaws and big
teeth). The following orthodontic abnormalities are hereditary: mandibular progenism, some types
of distal occlusion (pure distal occlusion and distal occlusion with the protrusion of upper incisors),
closed bite, cleft lip, jaw and palate, the abnormal number of teeth (hyperodontia, hypodontia or
anodontia), the abnormal shape and position of teeth (diastema, rotation) and the retention of
canines. Polygenic inheritance of orthodontic abnormalities is assumed, with some “threshold”, i.e.
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the phenotype manifestation will occur by the action of a greater number of genes of a small effect.
Interactions of such genes with external environmental factors also play an important role
(multifactorial inheritance).
To make a picture complete, it should be pointed out that “non-genetic” factors involved in the
development of orthodontic abnormalities also play an important role. They include factors that act
during the intrauterine development (teratogens, general diseases of the mother) and external
factors such as birth trauma, feeding, bad habits, the composition and consistence of food, the early
loss of temporary and permanent teeth, etc.
12.1.1 Disorders of the dentition
Hypodontia (one or more teeth are missing) is a very common disorder, affecting approximately 510% of population. It is usually associated with a predisposition with variable autosomal dominant
inheritance. Hypodontia and anodontia (all teeth are missing, it occurs very rarely) can also be part
of some genetic syndromes, for example X-linked hypohidrotic ectodermal dysplasia,
orofaciodigital syndrome, etc. The comprehensive examination of the patient is very important in
order to exclude associated problems and establish correct diagnosis and prognosis.
The most common developmental defects of teeth include defects of the formation of hard dental
tissue, particularly the enamel and dentin. Abnormalities in the formation of the enamel are caused
by defects that occur during the histodifferentiation, apposition or mineralization of the enamel
during development. Amelogenesis imperfecta is a well-known hereditary disease. The prevalence
of its different types is estimated to vary in a range of 1:14 000 - 1: 4 000. According to phenotype
manifestations, several different types of the disease can be distinguished (hypoplastic type,
hypomaturation type, hypocalcification type, hypoplastic/ hypomaturation type with taurodontism),
showing Mendelian inheritance (AD, AR and XR linked). The disease can be isolated or combined
with the symptoms of other syndromes (for example in tricho-dento-osseous syndrome – TDO,
Kohlschutter syndrome, etc.). There are also sporadic forms in which it is necessary to distinguish
non-genetic causes of the abnormal development of the enamel (fluorosis, tetracycline teeth due to
the use of tetracycline antibiotics, etc.)
Dentinogenesis imperfecta (DGI) and dentin dysplasia (DD) are typical examples of inherited
disorders of dentin formation. Dentinogenesis imperfecta can occur separately or as part of
different types of osteogenesis imperfecta. However, it should be pointed out that dentin
abnormalities can also be present in a number of systemic diseases associated with the defects of
the absorption and circulating levels of calcium and phosphates (for example vitamin D-resistant
rickets, hypoparathyroidism, etc.).
12.1.2 Jaw abnormalities
As mentioned above, a number of jaw abnormalities have a significant hereditary component.
Prognathism and mandibular progenism are the most common disorders.
Abnormalities of a prognathic origin (the excessive growth of the upper jaw) occur approximately
in 14% of population, multifactorial inheritance with a high correlation between siblings is
assumed.
Mandibular progenism is characterized by the enlargement of the lower jaw, usually in three
dimensions. The occurrence rate is 3-9% of population, inheritance is polygenic (multifactorial),
families with a characteristic AD type transfer were reported (the House of Habsburg is the best
example).
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12.1.3 Cleft lip and palate
Cleft lip and palate are relatively common congenital developmental defects. The detailed clinical
examination of a patient within genetic consulting is very important in order to exclude other
potentially associated abnormalities, and distinguish a multifactorial inherited isolated defect from
a number of genetic syndromes in which cleft lip and palate may also occur. The rate of isolated
cleft palate in the population varies in a range of 1/500-1/1000 whereas the rate of cleft palate is
approximately 1/2500.
Table 2
Cleft lip and palate – empirical risks (Harper)
Affected person
Sibling
Two siblings
Sibling and parent
Parent
Second-degree relative
Population risk
Cleft lip and palate
risk in %
2.2 – 4.0
10
10
4.3
0.6
0.3
0.1
Cleft palate
Risk in %
1.8
8
3
0.04
Table 3
Genetic risks for cleft lip and palate formation in connection with the seriousness of the
defect
Developmental defect
Bilateral cleft lip and palate
Unilateral cleft lip and palate
Unilateral cleft lip
Risk for a sibling in %
5.7
4.2
2.5
12.1.4 Some syndromes associated with cleft lip or cleft lip and palate
12.1.4.1 Autosomal dominant inheritance
– van der Woude syndrome (cleft defects of the face, paramedian lower lip fistula, hypodontia)
– EEC syndrome (ectrodactyly-ectodermal dysplasia- clefting syndrome)
– Stickler syndrome (hereditary progressive arthro-ophthalmopathy, i.e. arthro-ophtalmopathia
progressiva hereditaria)
– Larsen syndrome (arthrodigital syndrome)
12.1.4.2 Autosomal recessive inheritance
– Meckel syndrome
– Type II orofaciodigital syndrome
– Fryns syndrome
– Roberts syndrome (pseudothalidomide syndrome)
– Diastrophic dysplasia
– Smith-Lemli-Opitz syndrome
12.1.4.3 X-linked inheritance
– Type I orofaciodigital syndrome
– Otopalatodigital syndrome
– Isolated X-linked cleft palate with ankyloglossia
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12.1.4.4 Congenital chromosomal aberrations
Cleft lip and/or palate occur at a different rate in a large number of numerical or structural
chromosomal aberrations.
– Trisomy 13 (Patau syndrome)
– Trisomy 18 (Edwards syndrome)
– 4p- syndrome (Wolf-Hirschhorn syndrome)
– Microdeletion of 22q11- velocardiofacial syndrome, Di George syndrome
12.1.4.5 Syndromes without non-Mendelian inheritance
– Pierre Robin sequence – cleft palate, glossoptosis, micromandible
– Cleft defect with congenital heart defect
– De Lange syndrome
12. 2 Craniosynostoses and craniofacial syndromes
12.2.1 Craniosynostoses
Craniosynostoses form an etiologically and pathogenetically very heterogenic group. The disease is
characterized by the early closure of scull sutures with subsequent compensatory mechanisms
during the growth of scull bones. The disease can affect one or more scull sutures. It is either
isolated or combined with other abnormalities as part of syndrome units. It shows autosomal
dominant or autosomal recessive inheritance. In some sporadic cases, the role of external factors
cannot be excluded. About 70 syndromes have been described. The best known syndromes
include:
12.2.2 Autosomal dominant inheritance:
– Apert syndrome (gen fGfR2),
– Seathre-Chotzen syndrome (gen TWIST),
– Pfeiffer syndrome (gen fGfR2),
– Greig – cephalo-syndactyly (gen GLI3),
– Crouzon syndrome (gen fGfR2)
12.2.3 Autosomal recessive inheritance:
– Carpenter syndrome – acro-cephalo-syndactyly (lok.7p12)
12.2.4 Craniofacial syndromes
–
–
–
Treacher Collins syndrome (mandibulofacial dysostosis) – the syndrome has characteristic
facial features, eyelid coloboma, macrostomia, microgenia, rudimentary auricles, including the
typical hypoplasia and asymmetry of the facial skeleton. Autosomal dominant inheritance with
variable expressivity.
Hallermann-Streiff syndrome (oculo-mandibulo-dyscrania) – dyscrania with hypotrichosis,
facial abnormalities particularly in the eyes and short stature; the occurrence rate is usually
sporadic, autosomal dominant inheritance and autosomal recessive inheritance are assumed,
heterogenity?
Goldenhar syndrome (oculo-auriculo-vertebral complex, hemifacial microsomia) – facial
hypoplasia (usually unilateral), upper eyelid coloboma, epibulbar dermoid, rudimentary auricle,
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–
–
–
–
–
preauricular skin outgrowths, macrostomia, the abnormalities of the vertebrae. The occurrence
is usually sporadic; autosomal dominant and autosomal recessive inheritance including
polygenic inheritance is assumed in familial occurrences. The empirical risk of recurrence in
siblings is about 2-3%
Cleidocranial dysplasia (dysplasia cleidocranialis) – a characteristic defect of the skeleton
(scull, clavicle, pelvis) with typical facial features – the larger, wider and shorter brain part of
the scull with the protrudent forehead and parietal tubercles and the impression above the
glabella, the relatively small facial part of the scull with hypertelorism, the wide, deep root of
the nose and anteverted nostrils, both dentitions are delayed, supernumerary teeth. The narrow
chest with the hypoplasia or dysplasia of clavicles, hypermobile shoulders. Furthermore, the
narrow pelvis, thin limbs, somatic retardation from early age. Inheritance is autosomal
dominant, with high penetration but with significantly variable expressivity.
Orofaciodigital syndrome – a heterogenic group of defects including common minor facial
abnormalities, oral symptoms (cleft palate, lobed and cleft tongue, short frenulum, etc.) and
digital abnormalities such as brachydactyly, syndactyly, clinodactyly, polydactyly.
Approximately 8 types of the syndrome are distinguished (Type I has X dominant inheritance,
Type VIII has X- recessive inheritance, Types II-VI have autosomal recessive inheritance,
Type VII has autosomal dominant or X- dominant inheritance).
Oculodentodigital syndrome – a syndrome characterized by the narrow nose with hypoplastic
wings and thin nostrils, microcornea with abnormalities of the iris, syndactyly and/or
camptodactyly of postaxial fingers, the hypoplasia or aplasia of the medium phalanx of the 5 th
toe and by the hypoplasia of the enamel. Autosomal dominant inheritance, up to 50% of all
cases is due to new mutations.
Frontonasal dysplasia (median cleft face syndrome) – a developmental defect of heterogenic
etiology with symptoms such as hypertelorism, brachycephalia, the distinct forehead with the
broad root of the nose and more or less divided nose (usually with the frontal cranium bifidum
occultum and/or the median cleft face), usually with the open fontanel with open sutura
metopica and the synostosis of the coronary suture, facial asymmetry, high palate, diastematic
dentition. The occurrence is usually sporadic, autosomal dominant or recessive inheritance is
reported. The prevalence of the syndrome is 6:1 (females/males).
Aarskog’s syndrome (facial-digital-genital syndrome) – unusual facial features, short fingers,
somatic retardation, penoscrotal skin fold. Mild mental retardation which improves during
childhood. X recessive inheritance.
12.3 Dental caries
According to current opinions, dental caries arises due to complex interactions between three basic
factors: the susceptibility of dental tissue, the composition of oral microflora, and a diet. Time can
be considered the fourth factor since the carious process does not manifest itself immediately
clinically. Apart from the four above-mentioned basic factors, other influences have recently been
reported such as the individual resistance of the body against caries (affected by the amount and
composition of saliva). Inheritance plays a direct and indirect role in the formation of dental caries.
The direct role means that more resistant or less resistant tissue (the quality of the enamel) is
inherited. The indirect role of inheritance means that inheritance also determines the configuration
of teeth and the shape of dental crowns (the configuration of teeth with or without gaps, the depth
of fissures on the occlusal surface areas of premolars and molars, etc.). Due to the complex,
multifactorial nature of dental caries, it is assumed that the susceptibility or resistance to the
development of dental caries will result from complex interactions between genetic and
environmental factors. Such interactions have not yet been investigated.
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12.4 Diseases of the periodontium
Diseases of the periodontium are very common. Together with dental caries, they are a major
causes of the loss of teeth. Microbial plaque that accumulates on the surface of teeth is a substantial
link in the chain of causes resulting in the inflammations of periodontal tissue. Although the
presence of plaque bacteria seems to be an essential factor to initiate the inflammatory and immune
reaction of the body, it is not the only factor since the amount of plaque does not need to correlate
with the seriousness of a disease, which can be explained in terms of the individual susceptibility
to the disease. There is a large amount of data in literature supporting a key role of genes with
respect to immune response and the progression of the disease. More exactly, different allelic
variations of genes may lead to differences in the structure of tissue (natural immunity), antibody
response (acquired immunity) and the production of inflammatory mediators (non-specific
inflammation). Variations in these genes may act either as protective or as risk factors of the
disease. Currently, periodontitis is in most cases (except for rare, monogenic hereditary
“syndromological” forms, for example Papillon-Lefévre syndrome) considered to be a complex
disease whose phenotype is determined by both genetic and environmental factors that can affect
each other in synergy. Until now, the most general principles of the genetics of multifactorial
diseases (unlike the genetics of Mendelian diseases), have not been revealed. As a result, opinions
are still mixed in clinical practice regarding the results of genetic studies that have attempted to
reveal the genetic nature of multifactorial diseases, varying from over-optimistic expectations
about the identified “great effect” genes to deep scepticism. The interaction of the body genetic
basis with the conditions of the external environment is a very important feature of multifactorial
diseases. It should be emphasised that every new generation is born into “a different world” and it
is therefore necessary to do a very pragmatic assessment of the risks of genotypes of
multifactorially determined diseases for further generations.
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